dementia views you can use

Hope for dementia patients after Alzheimer's cells created in lab for first time Read more: http://www.dailymail.co.uk/health/article-2091716/Hope-dementia-patients-Alzheimers-cells-created-lab-time.html#ixzz1kWG64NIL

2012-01-29T08:22:00.001-05:00

More promising news on the Alzheimer's research front

2012-01-27T20:11:00.003-05:00

New strategies for treatment of disease of protein unfolding

2012-01-25T05:01:00.001-05:00

Bingo! Boost thinking skills and keep your mind healthy

2012-01-23T17:01:00.001-05:00

Here is a great dementia resource for caregivers and healthcare professionals,

You will love the Amazon Kindle Fire

Here is information on being the best caregiver you can be

Here is a way for nurses administrators, social workers and other health care professionals to get an easyceu or two

Follow Alzheimers1 on twitter

Examiner

Florence McGinn

Lifelong learning’s active mantra of “Use it or lose it” is boosted by new, perception research done by researchers from Case Western Reserve University, Boston University, and Bridgewater State University. Those university-based perception researchers found high-contrast, large bingo cards boosted thinking and playing skills for people with cognitive difficulties and visual perception problems produced by Alzheimer’s disease and Parkinson’s disease.

Active interventions

With research-based knowledge, productive interventions unfold. The university researchers indicate interventions connected to their studies work to allow individuals with mild dementia and others with visual perception deficits to achieve benefits that facilitate their basic abilities to live independently longer, perform daily tasks, and enjoy life’s simple pleasures.
The research findings were reported in the article, “Bingo! Externally supported performance intervention for deficit visual search in normal aging, Parkinson’s disease, and Alzheimer’s disease,” in the journal Aging, Neuropsychology, and Cognition. Concerning beneficial interventions, the researchers wrote, “The general finding of improved performance across healthy and afflicted groups suggests the value of visual support as an easy-to-apply intervention to enhance cognitive performance.”

Exploration needed in understanding connections

As people age, they begin to lose sensitivity to perceive contrasts. The perception problem is exacerbated in people with dementia, according to Grover C. Gilmore, a psychologist and dean of the Mandel School of Applied Social Sciences at Case Western Reserve University.

But, Gilmore, who has done extensive testing in his Perception Lab at Case Western Reserve, indicates, “Little is known about how visual perception problems—common in aging players—affect the way these people think and play.” Gilmore and the study’s lead investigator, Alice Cronin-Golomb from Boston University, have collaborated for two decades on projects that look at visual sensory deficits and cognition among people with dementia. For example, in individuals with Parkinson’s disease, driving is affected by low contrasts as demonstrated in simulated fog situations.

Bingo becomes a research tool

Bingo is often used in nursing homes and senior centers as a social activity, and being socially engaged helps keep the mind healthy. However, Bingo, a popular activity in nursing homes, senior centers and assisted-living facilities, has benefits that extend well beyond socializing.

Perception researchers tested Bingo cards of different sizes, contrasts and visual complexities to find out how visual perception problems impact cognitive functions among the study’s participants: 19 younger adults, 14 individuals with probable Alzheimer’s Disease, 13 Alzheimer’s Disease matched healthy adults, 17 non-demented individuals with Parkinson’s disease and 20 Parkinson’s disease-matched healthy adults.

When study participants played Bingo on computer-generated cards that were manipulated for brightness, size and contrast, the researchers could compare the performance among the different age and health groups.

Benefits in those with mild dementia

With some contrast and size changes to the cards, researchers reported improvement in performances. For those with mild dementia, they could perform at levels of their healthy peers. However, little change was reported for people with more severe dementia.

Living environment interventions

Boosting contrast is among interventions known as Externally Supported Performance Interventions (ESPI). Gilmore and Alice Cronin-Golomb found that boosting contrast in the living environment and also at the table enables people with dementia—who have lost the ability to distinguish between similar-contrast objects—to move safely around their homes and improve their eating.

For example, putting a black sofa in a white room would improve the contrast of the room and make it easier for individuals to move about. Additionally, they found that individuals with dementia actually eat more if they use a white plate and tableware on a dark tablecloth or are served food that contrasts the color of the plate.

Critical research

As more of the world’s population ages and experience age-related issues and diseases, understanding of interventions that can maintain or build mental capacities are critical. Cognitive difficulties can prove to be the silent epidemic that robs an aging population of final years that are active, productive, and meaningful. All of society benefits when systemic, cognitive process insights work to help keep brains active and healthy.

Alzheimer’s Disease: Managing Behavior Symptoms without Medication (part 2)

2012-01-21T05:01:00.001-05:00

Alzheimer’s Disease: Managing Behavior Symptoms without Medication

2012-01-19T05:02:00.000-05:00

USF researcher disputes Alzheimer’s as a disease

2012-01-17T05:02:00.000-05:00

Here is a great dementia resource for caregivers and healthcare professionals,

You will love the Amazon Kindle Fire

Here is information on being the best caregiver you can be

Here is a way for nurses administrators, social workers and other health care professionals to get an easyceu or two

Follow Alzheimers1 on twitter

Oracle

USF has been committed to finding a cure for Alzheimer's disease, with millions of dollars given or donated to the USF Health Byrd Alzheimer's Institute in the past year alone.
However, one researcher is convinced that money might be going to a cure that doesn't exist.
A recently published study in the Journal of Alzheimer's Disease by Ming Chen, an associate professor in the molecular pharmacology and physiology department, suggests that Alzheimer's in the elderly has no cure because it is not a disease, but rather a misnomer for a natural condition caused primarily by age.
"Over 20 years, I studied Alzheimer's," he said. "Then after the first 10 years, I started to realize that something might be wrong that turned things upside-down."
Chen said that neurotransmission, or the movement of signals sent through the brain, is regulated by calcium. While Chen expected calcium levels to decrease in a person with Alzheimer's because of the symptoms of impaired brain function, he found, as did the medical community at large, that calcium levels increased.
"From there, I realized something must be fundamentally wrong," he said. "This is due to advanced aging plus risk factor."
The study lists inactive lifestyles and unhealthy food as risk factors that increase a person's chances of getting Alzheimer's. While people can lessen their risk with exercise and a healthy diet, in the long run, he said people won't be able to escape Alzheimer's any more than they can escape death.
Chen said Alzheimer's is better categorized in terms of senile dementia and presenile dementia — dementia found in younger persons -— which he said is a disease. The causes of presenile dementia, three mutant genes, were not seen in senile dementia patients.
Chen likened the difference between senile and presenile dementia to the difference between hearing loss found in a member of the elderly and hearing loss found in a child.
"This is why we have geriatric medicine," he said. "For example, all people get hearing loss. That is due to aging, we all know that. However, if in young people there's lost hearing, then that must be disease, then that must be caused by a gene mutation or a virus or bacteria."
Chen said the controversial viewpoint isolated him from the medical community, as few scientists agree with him.
"There are a lot of (scientists) in USF, but I won't name any of them to avoid controversy," he said. "Our biggest challenge, is getting grant funding. To get a grant, you have to make a proposal and the proposal is reviewed by scientists in a field — a peer review. That's the problem. My views are different than the majority of the scientific community."
Dave Morgan, CEO of the USF Health Byrd Alzheimer's Institute, said Chen's argument has a few problems.
"Two names: George Burns and Betty White," he said. "So if it's normal aging, they should have it. They're both in their 90s, (and) they don't have it. So this is the problem with his argument. If it was from old age, everyone would have it."
Chen, however, said things are not so simple.
"It's like a radio in the car," he said. "You have an old radio, that radio will eventually die because of aging — not only radio, but the whole car will die. Not every (car) engine will overrun the radio's lifespan. There's always some cars dead with bad engine, with bad radio, but other cars dead with working radio. Alzheimer's will not affect everybody, no matter how long we live."
Huntington Potter, director of the Florida Alzheimer's Disease Research Center, said he agreed with Chen in regards to age itself being the No. 1 risk factor for developing Alzheimer's.
But Alzheimer's is a disease, he said, and all forms of disease are curable.
"I think a disease should be defined by any physiological process that is detrimental to health or happiness," he said. "So for any disease we seek scientists to prevent it or halt it or reverse its effects. And possibly all three."
Potter said the medical community should focus on understanding the effects of aging on the brain as to figure out the pathology, or cause, of the disease, and in doing so, "find a way to halt" Alzheimer's.
"We know quite clearly that it is very common for you to get Alzheimer's in your 80s, but it turns out if you reach the age of 100, your risks go down," Morgan said. "So that definitely proves that Alzheimer's is not a function of aging."

Meet the Mental Health Needs of Those With Dementia

2012-01-15T05:02:00.000-05:00

Here is a great dementia resource for caregivers and healthcare professionals,

You will love the Amazon Kindle Fire

Here is information on being the best caregiver you can be

Here is a way for nurses administrators, social workers and other health care professionals to get an easyceu or two

Follow Alzheimers1 on twitter

Huffington Post

People living with Alzheimer's or other dementias often have mental health problems -- especially depression and anxiety disorders -- as well as dementia. Memories they have always relied on become hazy and uncertain. Knowledge and skills cultivated over a lifetime diminish. Relationships change or are lost. Ordinary activities at work, home or leisure become difficult. Eventually, other people may be needed to help manage finances, make plans, get back and forth from home, eat, stay clean or go to the bathroom. As these sources of identity, personal pride and satisfaction are lost, people with dementia can become deeply sad, fearful and/or angry. Sometimes their behavior becomes a challenge for people who care for them.

These obvious facts should be part of what drives our nation's preparation for the vast growth of the number of people with Alzheimer's or other dementias that will take place over the next two decades.

The good news is that pursuant to The National Alzheimer's Project Act (NAPA) signed into law in January 2011, the U.S. Department of Health and Human Services (HHS) has begun to develop a long-term plan regarding dementia. The planning advisory committee for this project includes a representative of the Substance Abuse and Services Administration (SAMHSA) as well as representatives of many other federal agencies. In mid-December SAMHSA brought together a small group of experts who recommended that SAMHSA speak to the critical importance of addressing mental health problems experienced by people with dementia, Hopefully, it will do so at the next meeting of the advisory committee, which will take place on Jan. 17 and 18.

That's the good news. The bad news is that there is a battle shaping up about what the nation's priorities regarding dementia should be.

Some argue that there should be one and only one priority -- investing in research to discover a cure for Alzheimer's or at least to invent medications to stop the ineluctable decline the disease brings with it. For example, in an editorial in Alzheimer's and Dementia, Zaven Khachaturian of the Campaign to Prevent Alzheimer's Disease by 2020 argues, "Ultimately, the only deliverable that counts is a credible plan of action that calls for significant and systematic increases in the allocation of resources and funds for Alzheimer's research... particularly in the discovery and development of interventions to prevent disability."[1]

Others of us believe that, however promising biomedical research is, it will probably not bring relief in time for the 5.4 million Americans who already have dementia or for the additional five to six million people who will develop dementia over the next two decades. [2] We believe that humane care to help them have the best possible quality of life is the critical goal. We see this not as competing with biomedical research but as work that is necessary in addition to it.

But even among those of us who are focused on the need for more humane and more effective services and supports, there is some dispute about the importance of mental health services.

In part, this is the result of an outmoded view about the separation of mind and body. Dementia has physical roots with mental manifestations. Many advocates for better Alzheimer's care and treatment focus on the physical roots and do not regard dementia as a mental health condition. Others of us believe that mind and body are inextricably intertwined and that both physical and mental health perspectives and interventions are needed to help people with dementia and their families to have the best possible quality of life.

Many mental health issues arise in the lives of people with dementia and their caregivers. In a recent article in the same journal that published Khachaturian's editorial, Constantine Lyketsos and others argue that "neuropsychiatric symptoms (NPS) are core features of Alzheimer's disease and related dementias." They cite "depression and apathy ... verbal and physical agitation ... [and in later phases] delusions, hallucinations and aggression" as particularly common and important to address with mental health interventions, preferably non-pharmacological interventions. [3]

Psychological understanding can also contribute to improved quality of life for people with dementia and their families even if they do not have diagnosable mental illnesses. Dementia is often thought of as an unmitigated horror, but the truth is that some people with dementia lead lives that they find satisfying. Helping people with dementia to retain a sense of self-worth and be at peace with who they are is a very important goal for them. [4]

Mental health issues also touch family caregivers who provide 80 percent of the care for their relatives with disabilities. They are at high risk for depression, anxiety and physical illnesses that contribute to burn-out. Solid research by Mary Mittelman has shown that psychological support helps family caregivers live better with the stress they face, resulting in delay in nursing home placement by upward of 18 months. [5]

If the National Alzheimer's Plan does not reflect these facts, life for people with dementia and their families will end up far worse than it needs to be. That is why I and many others are advocating that the plan establish meeting the mental health needs of people with dementia and their families as a core priority for our nation.

More on Alzheimer's disease

References:

[1] Khachaturian, Z. "Prospects for designating Alzheimer's disease research a national priority" in Alzheimer's and Dementia, November 2011.

[2] Alzheimer's Association. "Facts and Figures About Alzheimer's."

[3] Lyketsos, C. et al. "Neuropsychiatric symptoms in Alzheimer's disease" in Alzheimer's and Dementia, September 2011.

[4] Zeisel, J. I'm Still Here. Avery Press, 2009.

[5] Mittelman, M. et al. "Improving Caregiver Well-Being Delays Nursing Home Placement of Patients with Alzheimer's Disease" in Neurology, November 14, 2006.

How nicotine patches could slow the onset of Alzheimer's disease

2012-01-13T05:03:00.001-05:00

Why do old people lose their memory

2012-01-11T05:03:00.001-05:00

Antioxidant found potentially valuable to fight Alzheimer's disease

2012-01-09T04:54:00.007-05:00

Antibodies may neutralize Alzheimer's

2012-01-07T05:26:00.000-05:00

A New Way to Detect Alzheimer's Disease

2012-01-05T09:42:00.000-05:00

New drug may stop the progression of Alzheimer's disease

2012-01-03T07:24:00.000-05:00

Here is a great dementia resource for caregivers and healthcare professionals,

You will love the Amazon Kindle Fire

Here is information on being the best caregiver you can be

Here is a way for nurses administrators, social workers and other health care professionals to get an easyceu or two

Follow Alzheimers1 on twitter

Medical News Today

According to findings in a study published in PLoS One, a new drug candidate may be the first drug that is capable of halting the devastating mental decline of Alzheimer's disease. Researchers administered the drug, known as J147, to mice with Alzheimer's disease and observed an associated improvement in memory and prevention in brain damage. The new drug was developed by scientists at the Salk Institute for Biological Studies, led by David Schubert, and could be trialled as a treatment for Alzheimer's disease in humans in the near future.

David Schubert, head of Salk's Cellular Neurobiology Laboratory, explained:

"J147 enhances memory in both normal and Alzheimer's mice and also protects the brain from the loss of synaptic connections. No drugs on the market for Alzheimer's have both of these properties."

The researchers say that even though the new compound's efficacy and safety in humans has not yet been established, the results indicate that the drug could become a potential treatment in people with Alzheimer's.  

  According to figures of the National Institutes of Health, a staggering 5.4 million Americans suffer from Alzheimer's. The Alzheimer's Association estimates that by 2050 more than 16 million will be affected by the disease, resulting in annual medical costs of over $1 trillion.  

Alzheimer's causes a steady, irreversible decline in brain function. Affected individuals experience a progressive loss of memory and ability to think clearly, which subsequently leads to the person being unable to perform simple tasks, such as eating and talking, and ultimately ends in death.

Alzheimer's is associated with aging, with a typical onset in individuals aged 60 years or above, although a small percentage of families carry a genetic risk for earlier onset. Amongst the top ten causes of mortality, Alzheimer's is the only disease that cannot be prevented, cured or reduced to progress slowly.

Onset of Alzheimer's seems to be influenced by a complex mixture of genetics, lifestyle factors and environment, although scientists still remain unclear what causes the disease. Until now, drugs developed for the treatment of Alzheimer's, such as Aricept, Razadyne and Exelon have only produced short periods of memory improvements, yet do not halt the overall progression of the disease.

Schubert and his team set out to find a new type of drug, but instead of following the current trend of the pharmaceutical industry, they decided to take a different approach. The pharmaceutical industry seems to focus exclusively on the biological pathways involved in the formation of amyloid plaques, the dense deposits of protein, which characterize the disease, but according to Schubert, until now, all amyloid-based drugs have failed in clinical trials.

Instead, they developed methods in which they used living neurons grown in laboratory dishes to assess the probability of whether or not new synthetic compounds prove effective in protecting the brain cells against several pathologies connected with brain aging. Based on the test results from each chemical iteration of the lead compound, a test originally designed for treating stroke and traumatic brain injuries, Schubert and his team managed to alter its chemical structure to produce a much more potent Alzheimer's drug.   

Marguerite Prior, a research associate in Schubert's lab, who led the project together with Qi Chen, a former Salk postdoctoral researcher, explained:

"Alzheimer's is a complex disease, but most drug development in the pharmaceutical world has focused on a single aspect of the disease - the amyloid pathway. In contrast, by testing these compounds in living cell cultures, we can determine what they do against a range of age-related problems and select the best candidate that addresses multiple aspects of the disease, not just one."

   The researchers subsequently tested their promising J147 compound as an oral medication in mice. In collaboration with Amanda Roberts, a professor of molecular neurosciences at The Scripps Research Institute, they performed a series of behavioral tests, which demonstrated that the drug improved memory in normal rodents.  

They subsequently demonstrated that J147 prevented cognitive decline in animals with Alzheimer's and also proved that mice and rats treated with the drug produced more of a protein called brain-derived neurotrophic factor (BDNF). BDNF is a molecule involved in memory formation and protects neurons from toxic insults. It also helps in the growths of new neurons and connects with other brain cells.

According to the researchers, based on the compounds broad ability to protect nerve cells, J147 may also be effective in the treatment of other neurological disorders, including Parkinson's and Huntingdon's disease as well as amyotrophic lateral sclerosis (ALS), and stroke.

The research was supported through funding by the Fritz B. Burns Foundation, the National Institutes of Health, the Bundy Foundation and the Alzheimer's Association.

Written by Petra Rattue

View drug information on ARICEPT; Exelon.

Copyright: Medical News Today

Helping those with dementia through comedy

2012-01-01T07:24:00.000-05:00

Small brain cortex may mean early dementia

2011-12-30T07:24:00.000-05:00

A New Way to Detect Alzheimer's Years Before Symptoms Appear

2011-12-28T07:24:00.001-05:00

Dementia linked to body's clock in elderly women

2011-12-26T07:17:00.001-05:00

(Here is a great dementia resource for caregivers and healthcare professionals,

You will love the Amazon Kindle Fire

Here is information on being the best caregiver you can be

Here is a way for nurses administrators, social workers and other health care professionals to get an easyceu or two

Follow Alzheimers1 on twitter

dailyRx)Dementia more often occurs in elderly women who are physically inactive, are active later in the day, or have abnormal sleep-wake schedules.

The group has an 80 percent higher chance of developing mild cognitive impairment (MCI) or dementia, says Greg Tranah, Ph.D., a scientist at the California Pacific Medical Center Research Institute in San Francisco. His team studied almost 1,300 women for five years.

Worried about memory loss? See a physician.
Most people's body clock, the circadian rhythm, helps wake them up between 6 a.m. and 8 a.m. They go to bed between 10 p.m. and 12 a.m. Normal rhythms vary for Individuals, but they are fairly regular.

In Dr. Tranah's study, women were less likely to develop dementia or MCI if they had strong circadian rhythm activity or were most physically active between 1:34 p.m. - 3:51 p.m..

The researchers collected data on activity and circadian rhythm from healthy women, all older than 75 (mean age 83). None lived in a nursing home or other group facility. No one had cognitive impairment or dementia when the study started.

After five years,15 percent of the women had developed dementia. MCI occurred in 24 percent. At highest risk were women with weaker circadian rhythm activity, lower levels of activity, or whose peak activity occurred after 3:50 p.m.

“We’ve known for some time that circadian rhythms can have an impact on the brain and the ability to function normally,” Dr. Tranah says. "This is the first study to show such a strong connection between circadian rhythm and the subsequent development of dementia or MCI."

No one knows why circadian rhythm and mental status are linked. A decrease in one might cause the other, says Dr. Tranah.

He says new research should study whether dementia and MCI rates improve after elderly women increase physical activity or use light to influence circadian rhythms.

Dr. Tranah and his team published their observational study in the Annals of Neurology.

Can you deduct the cost of a caregiver?

2011-12-24T07:25:00.003-05:00

Have a Merry Christmas with Great Gifts For Those With Dementia

2011-12-22T09:15:00.001-05:00

Here is a great dementia resource for caregivers and healthcare professinals,

Here is information on being the best caregiver you can be

Here are more interesting dementia brain boosting Corrier-journal.comactivities

Here is a dementia music activity

Learn what activities and gifts will make those with Alzheimer's disease or a related dementia smile this holiday season. These activities and gifts ensure you and your loved one or client a delightful Christmas, this year

PRLog – Over 5.4 million people in the US now have Alzheimer’s disease or a related dementia. We all benefit from sharing Christmas with someone we care about. The smells, the sounds, and the sights bring back happy memories. People with dementia should have this opportunity too. Following these tips will ensure you and your loved one with Alzheimer’s disease or another dementia a pleasurable holiday season. Use these tips to help you choose a gift they will enjoy now and in days and months to come.
The gift of yourself is one of the best gifts you can give so do things together.
One thing you can do .....read all of Great Gifts For Those With Dementia

Volunteers key to curing Alzheimer's disease

2011-12-20T04:10:00.002-05:00

Here is a great dementia resource for caregivers and healthcare professinals,

Here is information on being the best caregiver you can be

Here is a way for nurses administrators, social workers and other health care professionals to get an easyceu or two

Follow Alzheimers1 on twitter

NAPSI)—Although more than 5 million people age 65 and older in the U.S. are currently living with Alzheimer’s disease (AD), and while that number is expected to jump to 13.5 million by 2050, there is reason to hope. That’s good news for the almost 15 million more Americans—family members, friends, neighbors and volunteers—currently caring for their loved ones with AD without any real options to help them get better.

Alzheimer’s is the only disease in the top 10 causes of death without a way to prevent, cure or even slow the progression of the disease. In fact, between 2000 and 2008, deaths from AD increased by 66 percent, while deaths from HIV, stroke, heart disease and prostate cancer all declined significantly.

Scientists have learned a great deal about potential underlying causes of AD, and advancements in treatments have been accomplished in recent years. To spur more breakthroughs and speed discoveries, scientists are focusing on early detection through neuroimaging of the brain.

“We have to understand Alzheimer’s from its earliest signs in order to treat it effectively,” said Michael Weiner, M.D., principal investigator of the Alzheimer’s Disease Neuroimaging Initiative (ADNI). “If we can get a fuller picture of the brain and identify signs of the disease before someone gets ill, we can develop better treatment options, which could slow the progression and one day even prevent or cure Alzheimer’s.”

ADNI, the largest Alzheimer’s study of its kind, is now in its second phase (ADNI 2). Scientists are looking for volunteers ages 55−90 to participate in the study to allow them to continue their research at the pace needed to be successful against the disease. They are seeking healthy individuals, those with some memory concerns and people with diagnosed AD.

Participants will not only be contributing to the search for treatments and a cure for AD, they will also have the benefit of access to leading medical experts in the field. In many communities, it is difficult to find someone who knows specifically about Alzheimer’s disease, so clinical trials can be a great way to work with specialists.

“We cannot cure what we do not understand,” said Dr. Weiner. “But with the help of volunteers across the nation, we’re on the right path and making great strides to end the Alzheimer’s epidemic.”

To volunteer or learn more about the study, contact the National Institute on Aging’s Alzheimer’s Disease Education and Referral (ADEAR) Center at (800) 438-4380 or visit www.adni-info.org.

IV treatment for dementia

2011-12-18T05:26:00.002-05:00

Here is a great dementia resource for caregivers and healthcare professionals,

You will love the Amazon Kindle Fire

Here is information on being the best caregiver you can be

Here is a way for nurses administrators, social workers and other health care professionals to get an easyceu or two

Follow Alzheimers1 on twitter

Globe

In this year’s blockbuster Rise of the Planet of the Apes, a scientist reverses his father’s Alzheimer’s disease with a simple shot in the arm. The cure was temporary. But not entirely far-fetched.

Canadian scientists are working on an intravenous treatment for Alzheimer’s that could halt the progression of the disease and improve cognitive functions – without the risk of a mass ape revolt.

Vancouver researcher Neil Cashman and colleagues have discovered a biomarker on toxic molecules called amyloid-beta (a-beta) oligomers, which are catalysts in the brain degeneration of Alzheimer’s.

Their industry partner, Cangene Corp., a Winnipeg-based biopharmaceutical company, is developing antibodies designed to attack the toxic molecules without harming healthy ones.

If their work is successful, the antibodies could be used as an immune therapy for Alzheimer’s, or as a preventive vaccine, says Dr. Cashman, scientific director of PrioNet Canada, a network of centres conducting research into neurodegenerative disorders.

“We believe that we’ve found a target – perhaps the target – for treatment of Alzheimer’s disease,” he says.

Alzheimer’s is a neurodegenerative disorder, not an immune disease. Nevertheless, the immune system can be harnessed to defend against the harmful molecules involved in Alzheimer’s, says Dr. Cashman, a specialist in neurological diseases at the University of British Columbia.

He and other researchers at UBC and the University of Sherbrooke have found that selected antibodies will attack a-beta oligomers in cultured nerve cells. “It renders them non-toxic,” he says.

The next step is to test the treatment on mice engineered to develop Alzheimer’s. Mice studies will be completed at UBC and a lab in Milan, Italy, likely within three months, Dr. Cashman says.

If the work goes as planned, Cangene will begin developing an experimental treatment for clinical trials in humans, he says. “Cangene thinks it’s four years away.”

Immunotherapy for Alzheimer’s is a “very promising approach,” says Paul Aisen, a professor of neurosciences at the University of California, San Diego. But because various types of molecules may be involved in causing the disease, he says, “it’s not clear which precise targets are going to prove most useful.”

Alzheimer’s researchers have been testing different forms of immune therapy for some time. About a decade ago, Elan, a biotechnology company headquartered in Dublin, conducted human trials in the San Francisco Bay area using a vaccine against a-beta molecules. The trials were cut short in 2002 because 6 per cent of the patients developed meningoencephalitis, an inflammation of the brain that resulted in several deaths.

At the time, researchers concluded that the vaccine activated the immune system’s T cells, which attacked a-beta molecules in healthy nerve tissue.

But Dr. Cashman and his colleagues are developing a treatment that will target only a-beta oligomers, using the marker he has found. A-beta oligomers are widely accepted as a main source of neuron-harming toxicity in Alzheimer’s disease, he says.

Recent findings by other researchers suggest that immunotherapy may be a viable treatment, Dr. Cashman says. He points to human trials funded by Baxter International at institutions including the New York-Presbyterian Hospital/Weill Cornell Medical Center. In the multiphase trials, researchers are testing antibodies prepared from the blood of healthy plasma donors, known as intravenous immunoglobulin (IVIG), on patients with mild to moderate Alzheimer’s. “They’re getting remarkable results,” Dr. Cashman says.

In April, 2010, Baxter released unpublished findings of a phase II study showing that patients with Alzheimer’s who received IVIG had less brain atrophy and better cognitive functioning after 18 months compared with patients in a control group.

The Baxter trials are taking what some researchers call a “kitchen sink” approach to immunotherapy, giving patients a blood product containing all available human antibodies in hopes that some will be of benefit.

Instead, Cangene will select specific antibodies to develop an IVIG product with a “more concentrated effect,” Dr. Cashman says. Given Baxter’s success using unselected IVIG, he adds, “I think it’s actually going to work.”

But others are skeptical, and several Canadian specialists declined to comment on such early research.

Dr. Aisen cautions against jumping to conclusions based on the success of Baxter’s phase II study. Since only 14 patients received the full course of IVIG, the evidence that immunotherapy can halt Alzheimer’s is “too preliminary,” he says.

Dr. Aisen was not involved in the phase II trial, but he and colleagues at Alzheimer’s Disease Co-operative Study are conducting Baxter’s phase III trials using IVIG. The team has recruited 380 patients with mild to moderate Alzheimer’s for the third study, which is set for completion in about a year. Although the phase II results are encouraging, he says, “we really want to see the results of the larger study.”

In the meantime, Dr. Aisen suggests that lab experiments on cultured nerve cells and mice provide little evidence that a cure for Alzheimer’s is on the horizon.

“It’s a long way from a cell culture study to a human treatment,” he says

Transcending Dementia through the TTAP Method

2011-12-16T09:43:00.003-05:00

Simple way to fight Alzheimer's disease

2011-12-14T06:43:00.001-05:00

New Vaccine for Alzheimer's Disease

2011-12-12T09:43:00.001-05:00

Dementia risk is higher if you have.....

2011-12-10T04:09:00.001-05:00

Here is a great dementia resource for caregivers and healthcare professinals,

Here is information on being the best caregiver you can be

Here is a way for nurses administrators, social workers and other health care professionals to get an easyceu or two

Follow Alzheimers1 on twitter

HealthDay News -- Patients with diabetes who have comorbid depression are at increased risk for developing dementia compared with those with diabetes alone, study results indicate.

"Given that depression is potentially modifiable, future studies are needed to further evaluate whether effective depression interventions reduce the risk of dementia and identify the mechanisms that may explain our observation," Wayne Katon, MD, from the University of Washington in Seattle, and colleagues wrote in the Archives of General Psychiatry.

They surveyed a random sample of 19,239 patients with type 2 diabetes, aged 30 to 75 years, from the Diabetes and Aging Study to identify prevalent cases of depression. Dementia diagnoses were identified based on International Classification of Diseases, Ninth Revision-clinical modification [ICD-9-CM] criteria three to five years post-baseline to ensure that depression was not a prodrome of dementia. The researchers then estimated dementia risk for patients with depression and diabetes relative to patients with diabetes alone using Cox proportional hazard regression models adjusted for sociodemographic, clinical, risk factors and healthcare use.

One or more dementia diagnosis occurred in 2.1% of 3,766 patients with diabetes and comorbid depression, and in 1% of the 15,473 patients with diabetes alone (incidence rate=5.5 and 2.6 per 1,000 person-years, respectively), the researchers found. A 100% increased risk of dementia was observed in patients with comorbid depression (adjusted HR=2.02).

Previous studies have associated depression with poorer adherence to diet and exercise regimens, increased rates of cigarette smoking and higher HbA1c levels, according to the researchers, which could "worsen the course of diabetes and increase the risk of dementia associated with depression."

However, controlling for these potential confounding factors did not significantly change the risk for dementia among these patients. "These data suggest that biologic factors associated with depression may be important risk factors for dementia in patients with type 2 diabetes," the researchers wrote. They called for more studies to further examine potential mechanisms of action.

One of the study researchers disclosed financial ties to the pharmaceutical industry.

Katon W et al. Arch Gen Psychiatry. 2011; doi:10.1001/archgenpsychiatry.2011.154.

An apple a day should keep dementia at bay

2011-12-08T09:44:00.002-05:00

Top ten traveling tips when traveling with elderly family (part 4)

2011-12-06T05:15:00.004-05:00

Top ten traveling tips when traveling with elderly family (part 3)

2011-12-04T05:13:00.002-05:00

Top ten traveling tips when traveling with elderly family (part 2)

2011-12-02T05:12:00.002-05:00

Top ten traveling tips when traveling with elderly family

2011-11-30T04:10:00.001-05:00

Scientists discover additional Alzheimer's proteins in the tangles

2011-11-28T04:10:00.004-05:00

New Study Challenges Accepted Approaches to Research in Senile Dementia

2011-11-26T04:11:00.002-05:00

Here is a great dementia resource for caregivers and healthcare professionals,

You will love the Amazon Kindle Fire

Here is information on being the best caregiver you can be

Here is a way for nurses administrators, social workers and other health care professionals to get an easyceu or two

Follow Alzheimers1 on twitter

Health canal

Amsterdam, NL – Impacting millions of families and devouring billions of dollars globally, Alzheimer’s disease is the focus of exhaustive research to find a cure.

Although intensely investigated over the last three decades using cutting-edge technologies, the “pathogenic cause” of Alzheimer’s disease has not been found. While many research “breakthroughs” have been claimed and high-profile drugs trials carried out, why does the promised “cure” still seem to elude scientists?

In an effort to address this question, Ming Chen, PhD, Huey T. Nguyen, BS, and Darrell R. Sawmiller, PhD, Aging Research Laboratory, R&D Service, Bay Pines VA Healthcare System and University of South Florida, undertook an independent and systematic analysis of the underlying research assumptions against the established scientific principles. This analysis led them to hypothesize that perhaps the main problem is the research community’s perception of the disease.

In an article scheduled for publication in the December issue of the Journal of Alzheimer’s Disease the authors suggest that when the National Institutes of Health separated out dementia from other senile conditions and redefined it as a distinct and “curable” disease — Alzheimer’s – in the 1970s, it opened a Pandora’s box and may have misdirected research for decades. It triggered the search for pathogenic factors and cures, and disregarded the role of demographic change and its diverse end results in the elderly.

The authors argue that senile disorders – diseases occurring after age 60 and eventually affecting the majority of the elderly, such as tooth, hearing or memory loss – are caused by aging, thus differ fundamentally from distinct diseases by origin, study paradigm and intervention strategy.

Moreover, the authors contend that a central regulator in cognition − the Ca2+ signaling system − has been misconceived by institutional thinking that favors a “cure” for senile dementia. The dominant hypothesis, although unproven, is that Ca2+ levels rise throughout the aging process, leading to cell death, and thus research has focused on calcium antagonists to lower those levels. This viewpoint has been promoted by policy makers, and the subject of a number of high profile clinical trials, but to date no positive results have emerged.

In contrast, the authors propose that declining functionality of Ca2+ signaling as a result of the aging process, among a myriad of other age-related changes, leads to cognitive decline. Therefore interventions for senile dementia could activate Ca2+ function by promoting energy metabolism and also by Ca2+ agonists such as caffeine and nicotine. At the same time, risk factors play a key role. “Aging and Ca2+ deficits set the stage for senile dementia, but do not always lead to senile dementia in real life,” explains Dr. Chen. “Lifestyles and other risk factors are the key. So we think that senile dementia may be explained by ‘advanced aging plus risk factors.’ This model points to a new direction for prevention. This means we must support the elderly in healthy lifestyles. And we should develop medications to extend the lifespan of old neurons, rather than looking for ways to inhibit far-fetched ‘pathogenic’ factors.”

“The model implies that senile dementia is, by and large, a lifestyle disease,” says Dr. Chen. “This view, in fact, has been shared by many in the medical and clinical community, but contrasts sharply with current dominant theories in the Alzheimer research field, which assume a linear and ‘cause and effect’ mechanism. Since they have not taken into account the fundamental roles of aging and risk factors, it is clear that these theories, though highly appealing to the public and researchers alike, are of little relevance to the scientific nature of senile dementia.”

“The two overwhelming concepts, senile dementia as a distinct disease and the Ca2+ overload hypothesis, have effectively blocked any meaningful progress in senile dementia research, and have inhibited the self-correcting mechanism of science,” concludes Dr. Chen. “An independent scrutiny on the field may be helpful.”

“Although incurable”, Dr. Chen is optimistic. “Our research, if guided by correct theories, will produce medications to help delay dementia to a certain extent − similar to the drugs that delay or ameliorate atherosclerosis and osteoporosis today.”

Thanksgiving Activities For Those With Dementia

2011-11-22T07:36:00.003-05:00

Here is a great dementia resource for caregivers and healthcare professinals,

You will love the Amazon Kindle Fire

Here is information on being the best caregiver you can be

Here is a way for nurses administrators, social workers and other health care professionals to get an easyceu or two

Follow Alzheimers1 on twitter

How to Eat Right, Keep Calm and Enjoy Thanksgiving with Someone Who Has Alzheimer's Disease or a Related Dementia How to Eat Right, Keep Calm and Enjoy Thanksgiving with Someone Who Has Alzheimer's Disease or a Related Dementia

According to the National Institute of Mental Health(NIMH) over five million Americans are living with Alzheimer's disease or a related dementia. Countless others are impacted by their illness. Studies have shown that eating right staves off dementia and slows the decline of someone who already has Alzheimer's disease or another type of dementia.

What can you do as a friend, loved one, or health care professional, to make Thanksgiving enjoyable and healthy.

The first thing is to keep it simple. Do not make elaborate dishes that take lots of time. There are plenty of easy healthy recipes out there. Using South Beach Diet, Zone Diet or Weight Watchers recipes is a good place to start. You can modify the recipes according to the dementia persons' likes and dislikes.

Another tip is to involve persons with Alzheimer's disease or a related dementia. Ask them about their preferences. If they say that they do not know, help them by telling them about things you like. Say, for example, I like squash. How about you? Then talk about ways to make squash. In this way, you can discuss every item you want to have for Thanksgiving.

Have them help you prepare the food. Give dementia persons simple tasks to do. Of course, you need to know their strengths and weaknesses to choose an appropriate chore. Make sure the assignment is failure free. In other words, there is no right or wrong way to do it. While you are preparing the food, reminisce about past Thanksgivings. Do not ask: Do you remember when...? Rather say That was so much fun when we...

Have a good belly laugh while talking about the good old days. Remember, research indicates that laughter does make someone feel better.

Fill your home with pleasant soothing aromas. Making a soup before or after Thanksgiving is a good way to do this. Cook the soup on a low flame all day long to let those heavenly smells fill the air.

Do not have too many guests at the meal. Make sure to keep it low key.

You may want to have two Thanksgiving meals. One for you and one for them. The one for them need not be on Thanksgiving Day. Pick a day that you and the dementia person can spend the day together enjoying all the happiness has to offer.

Now that you have read about the tips for healthy dementia dining, go have a great day

The book Adorable Photographs of Our Baby makes a great holiday gift for someone with dementia

Facing the Key Challenges for Fighting Alzheimer's Disease

2011-11-20T04:11:00.001-05:00

Here is a great dementia resource for caregivers and healthcare professinals,

Here is information on being the best caregiver you can be

Here is a way for nurses administrators, social workers and other health care professionals to get an easyceu or two

Follow Alzheimers1 on twitter

WebMD

The Alzheimer's Association in a new report has identified 10 "critical challenges" that need to be addressed by the nation to combat the growth and devastating impact of Alzheimer's disease.

The challenges include lack of funding and problems with diagnosing Alzheimer's.

An estimated 5.4 million Americans are living with Alzheimer's now, and that number is expected to grow to 16 million by the year 2050, according to the Alzheimer's Association.

Because of this looming health crisis, President Obama signed into law the National Alzheimer's Project Act on Jan. 4, with the aim of creating a national strategic plan to address what the Alzheimer's Association described as an "escalating crisis."

The Alzheimer's Association's report, "Alzheimer's from the Frontlines: Challenges a National Alzheimer's Plan Must Address," was produced to help the government develop its strategy.

Findings of the report were based on input from 43,000 people in all 50 states, Puerto Rico, and Washington, D.C.

In all, the Alzheimer's Association hosted 132 public input sessions nationwide, involving people with Alzheimer's, caregivers, researchers, community leaders, and health care professionals.

"We want to make sure the administration is aware of the challenges that emerged, that we heard frequently, during the public input process," Alzheimer's Association spokeswoman Toni Williams tells WebMD. "We thought it would be a good idea to open it up to the public. We are hoping this helps to inform the advisory council and Secretary [Kathleen] Sebelius [of the U.S. Department of Health and Human Services] in formulating a plan."

When a Loved One Has Alzheimer's
Top Challenges in Fighting Alzheimer's

The 10 challenges highlighted by the Alzheimer's Association are:

Lack of public knowledge and awareness of the disease
Insufficient funding
Problems in detecting and diagnosing the disease
Poor dementia care
Inadequate treatments
Specific challenges faced by diverse communities
Specific challenges faced by those with younger-onset Alzheimer's
Unprepared caregivers
Ill-equipped communities
Mounting costs of care
The new report shows that costs relating to Alzheimer's care and treatment will surpass $1 trillion by mid-century unless the current trajectory of the disease changes.

"Individuals, families and communities are at the center of the escalating Alzheimer's crisis," Harry Johns, president and CEO of the Alzheimer's Association, says in a news release.

Call to Action

Americans who participated in the sessions aimed at identifying challenges want the nation's leaders to know that the disease changes lives, and that "they want and deserve a transformational plan that urgently addresses their needs," Johns says.

Robert Egge, vice president of the Alzheimer's Association, says the input sessions made it clear that people are not looking for symbolic acts but the start of "real, transformational action."

He says, "we hope those developing the National Alzheimer's Plan will be inspired and guided by the challenges, experiences and needs echoed throughout this report."

Egge says many Americans know little about the disease, and education is needed about warning signs of the disease and incorrect perceptions about it. Also, though the goal is a cure, better treatments are needed, he says, and more funding for research.

Currently, caregivers are isolated and uninformed about the disease. He says African-Americans and Hispanics are more likely to develop Alzheimer's, and less likely to be diagnosed.

The new plan, he says, "must address disparities in diverse and underserved communities.

Drink away Alzheimer's disease

2011-11-18T04:01:00.012-05:00

Here is a great dementia resource for caregivers and healthcare professinals,

Here is information on being the best caregiver you can be

Here is a way for nurses administrators, social workers and other health care professionals to get an easyceu or two

Follow Alzheimers1 on twitter

TheDenverChannel.com

TAMPA, Fla. -- Imagine slowly losing the sense of who you are and not being able to stop it. Millions of people in the U.S. live with Alzheimer's disease or watch a loved one suffers from it.

Now, researchers are looking at a high-powered prescription shake to ease the symptoms.

At 93, Teresa Alfonzo has seen and done a lot. But because of a devastating diagnosis 10 years ago, she's now fighting to keep her most precious "We started noticing she couldn't take care of herself," Rafael Alfonzo, Teresa's son, said.

The Alfonzo family is one of 35 million families dealing with the devastating effects of Alzheimer's disease. A few months ago, Teresa's ability to remember the most basic skills started to go. She couldn't even draw a clock.

"There was a lot of resistance. I don't understand," Margaret Alfonzo, Teresa's daughter, said.

That's when they decided to try something new. Teresa started on Axona, a medical shake regulated by the FDA. It's like an energy drink for the brain.

"It basically gives the brain an alternative food source," Richard S. Isaacson, M.D., an associate professor of clinical neurology at the University of Miami Miller School of Medicine

"It's a powder, so they mix it with usually a high protein drink, usually a milkshake or Boost, and they drink it right after breakfast," Susan Steen, M.D., a neurologist at South Tampa Memory center, said.

Alzheimer's patients lose the ability to use glucose in the blood. Two hours after drinking Axona, it's converted into ketone bodies that circulate to the brain and produce energy.

"Ketone bodies are the only things aside from sugar your brain can use as food." Dr. Richard S. Isaacson said.

In a 90-day, double blind study of 152 Alzheimer's patients, 77 took Axona. 45 percent of them showed signs of improvement after 45 days. While it doesn't work for everyone, Isaacson says it's worth a shot.

"You have at least a 40 to 45 percent chance of having this medical food work, in my opinion, 40 percent is a lot higher than zero," Isaacson said.

After three months on Axona, Teresa wa able to draw a clock.

"It's a blessing really. It's a huge progress," Margaret said.

Axona is a prescription medical food. The FDA does not approve medical foods, but they do regulate them. It costs $70 to $90 for a 30-day supply.

Isaacson says a genetic test can actually help figure out if Axona will work on patients. Axona's website says the side effects include mild stomach aches and diarrhea.

Yeast model connects Alzheimer's disease risk and amyloid beta toxicity

2011-11-16T04:33:00.001-05:00

Here is a great dementia resource for caregivers and healthcare professinals,

Here is information on being the best caregiver you can be

Here is a way for nurses administrators, social workers and other health care professionals to get an easyceu or two

Follow Alzheimers1 on twitter

EurekAlert

In a development that sheds new light on the pathology of Alzheimer's disease (AD), a team of Whitehead Institute scientists has identified connections between genetic risk factors for the disease and the effects of a peptide toxic to nerve cells in the brains of AD patients.

The scientists, working in and in collaboration with the lab of Whitehead Member Susan Lindquist, established these previously unknown links in an unexpected way. They used a very simple cell type—yeast cells—to investigate the harmful effects of amyloid beta (Aβ), a peptide whose accumulation in amyloid plaques is a hallmark of AD. This new yeast model of Aβ toxicity, which they further validated in the worm C. elegans and in rat neurons, enables researchers to identify and test potential genetic modifiers of this toxicity.

"As we tackle other diseases and extend our lifetimes, Alzheimer's and related diseases will be the most devastating personal challenge for our families and one the most crushing burdens on our economy," says Lindquist, who is also a professor of biology at Massachusetts Institute of Technology and an investigator of the Howard Hughes Medical Institute. "We have to try new approaches and find out-of the-box solutions."

In a multi-step process, the researchers were able to introduce the form of Aβ most closely associated with AD into yeast in a manner that mimics its presence in human cells. The resulting toxicity in yeast reflects aspects of the mechanism by which this protein damages neurons. This became clear when a screen of the yeast genome for genes that affect Aβ toxicity identified a dozen genes that have clear human homologs, including several that have previously been linked to AD risk by genome-wide association studies (GWAS) but with no known mechanistic connection.

With these genetic candidates in hand, the team set out to answer two key questions: Would the genes identified in yeast actually affect Aβ toxicity in neurons? And if so, how?

To address the first issue, in a collaboration with Guy Caldwell's lab at the University of Alabama, researchers created lines of C. elegans worms expressing the toxic form of Aβ specifically in a subset of neurons particularly vulnerable in AD. This resulted in an age-dependent loss of these neurons. Introducing the genes identified in the yeast that suppressed Aβ toxicity into the worms counteracted this toxicity. One of these modifiers is the homolog of PICALM, one of the most highly validated human AD risk factors. To address whether PICALM could also suppress Aβ toxicity in mammalian neurons, the group exposed cultured rat neurons to toxic Aβ species. Expressing PICALM in these neurons increased their survival.

The question of how these AD risk genes were actually impacting Aβ toxicity in neurons remained. The researchers had noted that many of the genes were associated with a key cellular protein-trafficking process known as endocytosis. This is the pathway that nerve cells use to move around the vital signaling molecules with which they connect circuits in the brain. They theorized that perhaps Aβ was doing its damage by disrupting this process. Returning to yeast, they discovered that, in fact, the trafficking of signaling molecules in yeast was adversely affected by Aβ. Here again, introducing genes identified as suppressors of Aβ toxicity helped restore proper functioning.

Much remains to be learned, but the work provides a new and promising avenue to explore the mechanisms of genes identified in studies of disease susceptibility.

"We now have the sequencing power to detect all these important disease risk alleles, but that doesn't tell us what they're actually doing, how they lead to disease," says Sebastian Treusch, a former graduate student in the Lindquist lab and now a postdoctoral research associate at Princeton University.
Jessica Goodman, a postdoctoral fellow in the Lindquist lab, says the yeast model provides a link between genetic data and efforts to understand AD from the biochemical and neurological perspectives.

"Our yeast model bridges the gap between these two fields," Goodman adds. "It enables us to figure out the mechanisms of these risk factors which were previously unknown."

Members of the Lindquist lab intend to fully exploit the yeast model, using it to identify novel AD risk genes, perhaps in a first step to determining if identified genes have mutations in AD patient samples. The work will undoubtedly take the lab into uncharted territory.

###
Notes staff scientist Kent Matlack: "We know that Aβ is toxic, and so far, the majority of efforts in the area of Aβ have been focused on ways to prevent it from forming in the first place. But we need to look at everything, including ways to reduce or prevent its toxicity. That's the focus of the model. Any genes that we find that we can connect to humans will go into an area of research that has been less explored so far."

This work was supported by an HHMI Collaborative Innovation Award, an NRSA fellowship, the Cure Alzheimer's Fund, the National Institutes of Health, the Kempe foundation, and Alzheimerfonden.

Susan Lindquist's primary affiliation is with Whitehead Institute for Biomedical Research, where her laboratory is located and all her research is conducted. She is also a Howard Hughes Medical Institute investigator and a professor of biology at Massachusetts Institute of Technology.

Full Citation:

"Functional Links Between Aβ Toxicity, Endocytic Trafficking and Alzheimer's Disease Risk Factors in Yeast"

Sebastian Treusch (1,2), Shusei Hamamichi (1,3), Jessica L. Goodman (1), Kent E.S. Matlack (1,2), Chee Yeun Chung (1), Valeriya Baru (1,2), Joshua M. Shulman (4,5), Antonio Parrado (6), Brooke J. Bevis (1), Julie S. Valastyan (1,2), Haesun Han (1), Malin Lindhagen-Persson (7), Eric M. Reiman (8,9), Denis A. Evans (10), David A. Bennett (11), Anders Olofsson (7), Philip L. DeJager (4,5), Rudolph E. Tanzi (6), Kim A. Caldwell (3), Guy A. Caldwell (3) and Susan Lindquist (1,2)

Whitehead Institute for Biomedical Research, Cambridge, MA 02142, USA.
Howard Hughes Medical Institute, Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02139.
Department of Biological Sciences, The University of Alabama, Tuscaloosa, AL 35487.
Program in Translational NeuroPsychiatric Genomics, Institute for the Neurosciences, Departments of Neurology & Psychiatry, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115.
Program in Medical and Population Genetics, Broad Institute, Cambridge, MA 02142.
Genetics and Aging Research Unit, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA 02129.
Department of Medical Biochemistry and Biophysics, Umea University, Umea, Sweden.
Neurogenomics Division, Translational Genomics Research Institute and Arizona Alzheimer's Consortium, Phoenix, AZ 85004.
Banner Alzheimer's Institute and Department of Psychiatry, University of Arizona, Phoenix, AZ 85006.
Rush Institute for Healthy Aging, Department of Internal Medicine, Rush University Medical Center, Chicago, IL 60612.
Rush Alzheimer's Disease Center, Department of Neurological Sciences, Rush University Medical Center, Chicago, IL 60612.

Eye Surgery Improves Mood of Alzheimer's Patients(part 2)

2011-11-14T04:33:00.000-05:00

Eye Surgery Improves Mood of Alzheimer's Patients

2011-11-12T04:33:00.004-05:00

Here is a great dementia resource for caregivers and healthcare professinals,

Here is information on being the best caregiver you can be

Here is a way for nurses administrators, social workers and other health care professionals to get an easyceu or two

Follow Alzheimers1 on twitter

WebMD

Study Shows Alzheimer's Patients May Sleep Better, Be Less Depressed After Cataract Surgery
By Charlene Laino
WebMD Health News Reviewed by Laura J. Martin, MD

People with Alzheimer's disease should have regular eye tests to screen for vision problems.

That's the recommendation of researchers who found that people with mild Alzheimer's disease who have cataracts may benefit from vision-correcting surgery. The benefits include improved sight, better sleep, and less depressed mood.

Also, people with Alzheimer's often had better communication and interaction with others after the surgery.

According to Brigitte Girard, MD, a professor of ophthalmology at Tenon Hospital in Paris, treatment improved the patients' lives and also the lives of some caregivers.

Girard reported the researchers' findings at the annual meeting of the American Academy of Ophthalmology (AAO) at the end of October.

Despite fears to the contrary, Girard says, surgery did not worsen patients' general condition or dementia.

William Thies, PhD, scientific director of the Alzheimer's Association, reviewed the findings for WebMD. He says that general medical care, including vision problems, are often overlooked in people with Alzheimer's.

"The assumption is made they won't benefit," Thies says. The assumption, he adds, is wrong. "The fact that they do benefit is very much the message from this study."

Improvements in Mood and Sleep

More than 1.5 million cataract surgeries are performed annually in the U.S. One in three Americans, most of them older people, will have the surgery at some point in their life.

The surgery is performed to remove the natural lens of the eye, which sometimes becomes clouded over time. A permanent artificial lens is then implanted to replace the natural lens.

The study involved 38 people with mild Alzheimer's disease who underwent cataract surgery. The average age was 86; nine were 90 or older. The majority (82%) were women.

Three months after surgery, all but one patient could see better. Three in four patients had improved or unchanged scores on tests of mood, memory, and their ability to wash, dress, and otherwise function independently. Sleep, in particular, improved, Girard says.

Six of the seven people with depression before surgery were less depressed afterward. The other person's depression was about the same as before.

As rated by the patients and their caregivers, social lives improved or were unchanged in two out of every three people studied.

Girard says "unchanged" scores were considered a mark of success. "As one neurologist told me," she says, "if people with Alzheimer's disease don't get worse over three months, it's a win."

The researchers did find that some people were more agitated after the surgery.

Benefits for Caregivers

The study also found that the surgery eased the burden for one in four caregivers. For another one in four, though, caring for their loved one was harder. The main reason cited was an increased level of agitation.

Sleep Disorders Lead To Increased Dementia Risk

2011-11-10T06:06:00.000-05:00

Here is a great dementia resource for caregivers and healthcare professinals,

Here is information on being the best caregiver you can be

Here is a way for nurses administrators, social workers and other health care professionals to get an easyceu or two

openPR

Older women with sleep-disordered breathing are more likely to develop cognitive impairment or dementia than women without this disorder according to a new study.

According to medical researchers, sleep-disordered breathing is a condition where the person has recurrent arousals from sleep and intermittent hypoxemia. "This condition can be common among older people and affects up to 60 percent of the elderly population," explains Jesse Slome, director of the American Association for Long Term Care Insurance.

Health experts report that the condition has been linked to various adverse health problems including hypertension, cardiovascular disease and diabetes. Researchers at the University of California, San Francisco, investigated the link between prevalent sleep-disordered breathing measured and the subsequent diagnoses of mild cognitive impairment and dementia.

The study tested nearly 300 women who were the average age of 82.3 years. The participants were without dementia at the start of the study. The participants' cognitive status was ranked as normal, dementia, or mild cognitive impairment. The study examined measures of hypoxia, sleep fragmentation and sleep duration as underlying mechanisms for any link between sleep-disordered breathing and cognitive impairment.

According to the study, some 35.2 percent of the tested women met the criteria for sleep-disordered breathing. Nearly an equal amount, some 35.9 percent of the women, developed mild cognitive impairment (20.1 percent) or dementia (15.8 percent) after an average follow up of 4.7 years. The study revealed, 47 of women (44.8 percent) with sleep-disordered breathing acquired mild cognitive impairment or dementia in comparison with 31.1 percent of those without sleep-disordered breathing.

Cognitive decline and dementia is a leading reason that aging senior women ultimately require costly long term care, Slome acknowledges. "Long term care insurance can pay for qualifying care at home or in a skilled nursing home but you must apply well before a decline in mental ability or physical health takes place," he notes.

The dangers of your aging parent covering up dementia (part 3)

2011-11-08T07:30:00.000-05:00

Here is a great dementia resource for caregivers and healthcare professinals,

Here is information on being the best caregiver you can be

Here is a way for nurses administrators, social workers and other health care professionals to get an easyceu or two

Forbes

Carolyn Rosenblatt

TO DO LIST
1. Persuade Dad to get a checkup from a reliable MD, preferably a neurologist who deals with aging patients.

You need information. If there are symptoms of dementia, you need to find out what’s going on. If other conditions are in play, appropriate care may make a difference. If you have to conspire with the doc in advance, do it.

2. Locate and update all estate planning documents. Work with your parents on this. Trusts, wills, durable powers of attorney and health care directives are the most important ones you need to review. It might have been years since anyone looked them over. Urge your parent to see an estate planning attorney. Tax laws change, state laws can vary. Some aging parents have never actually gotten the necessary legal papers together. The time may come when Dad is no longer competent to sign anything. Waiting until “the right time” is not good strategy. It can be too late before you know it.

3. Plan ahead for Dad’s possible care needs. Who would look after him if Mom could no longer do this? He may go downhill in the future. If he does have dementia, it won’t remain the same over time. People get more dependent on help with their daily needs. Help is not free. Some source of payment for help with daily care should be in the plan.

4. Discuss Dad’s situation with all family members. Call a family meeting. If Dad has memory problems now, everyone in the family will eventually be involved in the situation. Siblings may need to share caregiving duties. Some may need to make financial contributions. Taking care of both parents as they age is no longer rare. An honest conversation about who can do what, and who is willing to help aging parents can go a long way toward avoiding resentment and conflict later on. Take the first step. Be the leader. Someone has to do this, and it isn’t always an aging parent.

You don’t want to be the one lulled into a false sense of security because no one has officially diagnosed your aging parent with a specific kind of dementia. It doesn’t matter. Trust your own eyes and ears. If your gut tells you there’s something wrong here with your loved one, there probably is something wrong. Jaclyn already knows something is brewing with her Dad. She’s being proactive and I applaud her.

You’re not alone if you have a parent with memory loss. Millions of people are facing this every day. They find a way to manage it, and survive and you will too. Be smart. Look down the road. Stand tall and do this last part of being a grown child of your parent. Take the basic steps to protect your aging parent and yourself and you will get through it without unnecessary stress.

Support Veteran's with dementia this Veteran's Day

2011-11-06T03:34:00.001-05:00

Here is a great dementia resource for caregivers and healthcare professinals,

Here is information on being the best caregiver you can be

Here is a way for nurses administrators, social workers and other health care professionals to get an easyceu or two

Follow Alzheimers1 on twitter

Veterans who suffer from various forms of dementia, including Alzheimer disease, often have very specific care needs. It is important that these veterans are cared for by people who understand their condition and have the appropriate instruction and skills.

Therefore encourage family members of veterans to gain the training they need to care for their loved one with dementia.

For those in nursing homes and other institutions, make sure veterans with dementia are visited often.

All people, including those with memory loss, need human contact. They need to be hugged. They need to hear your voice. They may not know you but as long as you know who they are, that's all that matters.

Talk to them about their service to our country. Often they will share stories with you because their time in the service made a huge impression on them

Tell them how proud you are of them. Thank them for their service. This is sure to make them feel good. Most likely, it will make them smile

Smile with a veteran. Laughter is wonderful medicine...

Sing patriotic songs with a veteran with dementia. Often they will be able o sing many familiar songs even though, they may not be able to speak.

Read to them. Have them read to you. Large simple statements are best.

Share pictures with them, especially large colorful ones

Make a visitor’s packet for them.

For more ideas on things you can do with a veteran or anyone with dementia on this Veteran's Day or any day, read the book, Adorable Photographs of Our Baby-Meaningful, Mind-Stimulating Activities and More for the Memory Challenged, Their Loved Ones, and Involved Professionals

Abnormal Protein May Explain Loss of Smell With Alzheimer’s

2011-11-04T00:14:00.001-04:00

Here is a great dementia resource for caregivers and healthcare professinals,

Here is information on being the best caregiver you can be

Here is a way for nurses administrators, social workers and other health care professionals to get an easyceu or two

Follow Alzheimers1 on twitter

Doctor's Lounge

The protein kills nerve cells in the nose, animal study finds.

(HealthDay News) -- A loss of a sense of smell can be one of the earliest signs of Alzheimer's disease.

New research suggests that an abnormal form of a protein -- amyloid precursor protein, or APP -- which has been previously associated with the Alzheimer's disease may be to blame.

A study in mice found that animals genetically engineered to produce high levels of the abnormal protein experienced high levels of death in nerve cells in their nose compared to normal mice.

Researchers say the findings may explain why people suffering from the progressive illness often lose their sense of smell while the disease is still in its initial stages. They added this new insight might help doctors detect the condition early on.

"Deficits in odor detection and discrimination are among the earliest symptoms of Alzheimer's disease, suggesting that the sense of smell can potentially serve as a canary in the coal mine for early diagnosis of the disease," study leader Leonardo Belluscio of the U.S. National Institute of Neurological Disorders and Stroke, said in a news release.

"The changes taking place in the olfactory system as a result of Alzheimer's disease may be similar to those in other regions of the brain but appear more rapidly," he added.

APP has been detected in the nose nerve cells of some people with early onset Alzheimer's, a rare form of the disease that runs in families and strikes before age 65.

The researchers found mice making the mutated form of APP had four times as much olfactory nerve cell death at three weeks of age than normal mice.

When researchers blocked the production of high levels of the mutated protein, more olfactory nerve cells survived.

"Reducing APP production suppressed the widespread loss of nerve cells, suggesting that such disease-related death of nerve cells could potentially be stopped," explained Belluscio.

The study, published in the Sept. 28 issue of The Journal of Neuroscience, also found that the cells that died in the nose did not contain amyloid plaques, which are derived from APP. Plaques have long been believed to contribute to the death of nerve cells in the brains of people with Alzheimer's, leading to memory loss.

The researchers say the findings suggest that APP itself may be responsible for the death of nerve cells.

"Together, these results support the hypothesis that amyloid proteins are involved in the degeneration of the brain that occurs with Alzheimer's disease," Donald Wilson of New York University School of Medicine and the Nathan Kline Institute for Psychiatric Research, said in a news release from the journal.

"Further, they provide an exciting opportunity to explore how to prevent or reverse the events that lead to cell death and, ultimately, dementia," added Wilson, an olfactory system expert who was not involved in the study.

While more research is needed, it should be noted that studies involving animals often fail to produce similar results with humans.

More information

The National Institutes of Health provides more information on Alzheimer's disease.

SOURCE: Society for Neuroscience, news release, Sept. 27, 2011

New research targets treatment for dementia

2011-11-02T00:15:00.001-04:00

Here is a great dementia resource for caregivers and healthcare professinals,

Here is information on being the best caregiver you can be

Here is a way for nurses administrators, social workers and other health care professionals to get an easyceu or two

Follow Alzheimers1 on twitter

msn news

From Surabhi Gupta(PTI)

People suffering from dementia can heave a sigh of relief as neuroscientists in Australia have discovered a fundamental component of the process that regulates memory formation.

Neuroscientists at the Queensland Brain Institute (QBI) of The University of Queensland discovered the component in the hippocampus � a part of the brain commonly associated with memory function.

The discovery explains, for the first time, how new nerve cells form in this area of the brain associated with learning and memory � which deteriorate in people with stroke and dementia, QBI Director Professor Perry Bartlett told PTI.

"The hippocampus is the region of the brain involved in important functions such as learning and memory, and loss of neuronal production in the hippocampus is associated with a range of neurodegenerative conditions. It is particularly evident in ageing dementia," Bartlett said.

"Surprisingly, however, studies so far have failed to identify a resident stem cell population in the hippocampus that''s capable of providing the renewable source of these essential nerve cells."
Research by Professor Bartlett and his QBI colleagues, Dr Tara Walker and Dr Dhanisha Jhaveri (a recipient of the Indian National Science Academy''s award for Young Scientist of the Year 2003), has identified the resident populations of stem cells in the hippocampus.

Even more importantly, this research has discovered how it can be activated to produce new neurons.

The discovery of the presence of precursors in the adult brain which have the potential to produce neurons via a process called neurogenesis, will help immensely in the case of dementia patients, Bartlett said.

"For the first time, we''ve been able to identify a mechanism that''s able to regulate production of nerve cells, a step that''s crucial to our understanding of memory and learning," Professor Bartlett said.

"The same mechanism helps regulate growth of healthy brain tissue, so identifying this process is essential for the development of therapeutics to treat conditions such as dementia and depression."
A detailed understanding of the activation process should enable the development of therapeutics that can stimulate the production of new neurons and reverse or prevent the cognitive decline that occurs during ageing dementia, he said.

"These significant advances in determining the molecular regulation of nerve production will also have a major impact on our understanding of more complex areas such as behavior, cognition, neurological disease and mental illness," he added.

He said that the latest research provides further evidence that the mammalian central nervous system has the potential capacity to respond to its outside environment by generating new nerve cells.

The QBI research augments ongoing efforts to identify cellular and molecular mechanisms that can repair compromised brain tissue, and represents another milestone in understanding the fundamental workings of the brain.

Alzheimer's may originate in a form similar to that of infectious prion diseases

2011-10-31T00:16:00.002-04:00

Here is a great dementia resource for caregivers and healthcare professinals,

Here is information on being the best caregiver you can be

Here is a way for nurses administrators, social workers and other health care professionals to get an easyceu or two

Follow Alzheimers1 on twitter

news-medical.net

The brain damage that characterizes Alzheimer's disease may originate in a form similar to that of infectious prion diseases such as bovine spongiform encephalopathy (mad cow) and Creutzfeldt-Jakob, according to newly published research by The University of Texas Health Science Center at Houston (UTHealth).

"Our findings open the possibility that some of the sporadic Alzheimer's cases may arise from an infectious process, which occurs with other neurological diseases such as mad cow and its human form, Creutzfeldt-Jakob disease," said Claudio Soto, Ph.D., professor of neurology at The University of Texas Medical School at Houston, part of UTHealth. "The underlying mechanism of Alzheimer's disease is very similar to the prion diseases. It involves a normal protein that becomes misshapen and is able to spread by transforming good proteins to bad ones. The bad proteins accumulate in the brain, forming plaque deposits that are believed to kill neuron cells in Alzheimer's."

The results showing a potentially infectious spreading of Alzheimer's disease in animal models were published in the Oct. 4, 2011 online issue of Molecular Psychiatry, part of the Nature Publishing Group. The research was funded by The George P. and Cynthia W. Mitchell Center for Research in Alzheimer's Disease and Related Brain Disorders at UTHealth.

Alzheimer's disease is a form of progressive dementia that affects memory, thinking and behavior. Of the estimated 5.5 million cases of Alzheimer's in the United States, 90 percent are sporadic. The plaques caused by misshapen aggregates of beta amyloid protein, along with twisted fibers of the protein tau, are the two major hallmarks associated with the disease. Alzheimer's is the sixth leading cause of death in the United States, according to the Alzheimer's Association.

Researchers injected the brain tissue of a confirmed Alzheimer's patient into mice and compared the results to those from injected tissue of a control without the disease. None of the mice injected with the control showed signs of Alzheimer's, whereas all of those injected with Alzheimer's brain extracts developed plaques and other brain alterations typical of the disease.

"We took a normal mouse model that spontaneously does not develop any brain damage and injected a small amount of Alzheimer's human brain tissue into the animal's brain," said Soto, who is director of the Mitchell Center. "The mouse developed Alzheimer's over time and it spread to other portions of the brain. We are currently working on whether disease transmission can happen in real life under more natural routes of exposure."

Source: University of Texas Health Science Center at Houston

Blood Test Predicts Course of Alzheimer's

2011-10-29T00:17:00.001-04:00

Here is a great dementia resource for caregivers and healthcare professinals,

Here is information on being the best caregiver you can be

Here is a way for nurses administrators, social workers and other health care professionals to get an easyceu or two

Follow Alzheimers1 on twitter.

By Crystal Phend, Senior Staff Writer, MedPage Today

Reviewed by Robert Jasmer, MD; Associate Clinical Professor of Medicine, University of California, San Francisco and
Dorothy Caputo, MA, RN, BC-ADM, CDE, Nurse Planne

Plasma levels of sphingolipid compounds can predict progression of Alzheimer's disease, a small, early, observational study showed.

Higher ratios of sphingomyelins to ceramide and of dihydrosphingomyelin to dihydroceramides predicted significantly slower clinical progression, Michelle M. Mielke, PhD, of Johns Hopkins University, and colleagues found. Mielke is now at Mayo Clinic in Rochester, Minn.

If validated, sphingolipids could be "a sensitive, and easily accessible, biomarker" for Alzheimer's progression, they reported online in the Journal of Alzheimer's Disease.

That would be a big advantage for families and caregivers and also may help in development of better treatments for Alzheimer's, the group suggested.

Sphingolipids play a critical role in cellular signaling as major components of cell membranes, particularly in the central nervous system, where the proper balance of different species of these fats is essential for normal function of neurons.

The researchers correlated sphingolipid levels measured in 120 patients with probable Alzheimer's disease, predominantly of mild to moderate severity, at a single center. They were followed for progression over 2.3 years on average.

Higher levels of the various sphingolipids didn't predict more severe dementia at baseline, but they did predict rate of decline.

Higher dihydroceramides predicted significantly greater decline on the Mini-Mental State Exam (MMSE, P=0.050 as a continuous variable), while ceramides showed a similar but nonsignificant trend.

On the other hand, plasma sphingomyelins at higher levels predicted less progression on the MMSE (1.15 points difference for highest versus lowest tertile, P=0.006).

The same was true for dihydrosphingomyelin, with the top tertile progressing by 0.84 fewer points than those in the bottom tertile (P=0.046).

But the strongest predictors were ratios of metabolically-linked pairs of these lipids.

Ceramides are both a precursor for sphingomyelins and can be formed by their catabolism, and the same is true for the dihydro form of both.

The ratio of sphingomyelins to ceramides was associated with 1.19-points less decline on the MMSE (P=0.004) and 2.42-points less worsening on the Alzheimer's Disease Assessment Scale-Cognitive Subscale for the top versus bottom tertile (P=0.016).

The ratio of dihydrosphingomyelins to dihydroceramides correlated with a decline of 1.35 fewer points on the MMSE and an increase of 3.18 fewer points on the cognitive scale (both P=0.001).

"Together, these results suggest a shift in the metabolic pathways from ceramide to sphingomyelins over the course of Alzheimer's disease," such that the ratios may be useful predictors of clinical progression in later stages of the disease, Mielke's group suggested in the paper.

Total cholesterol and triglycerides didn't predict progression of Alzheimer's disease.

The researchers also looked at correlation of all the factors with functional decline measured on the Clinical Dementia Rating-Sum of Boxes but found no significant predictors.

They cautioned that the lipid levels measured at baseline weren't taken while fasting, which may have affected levels of some plasma sphingolipids.

But controlling for body mass index, diabetes and cardiovascular disease status, as well as other factors in the individuals in whom they were known didn't appear to impact the results.

The study was funded by a grant from George P. Mitchell and the late Cynthia W. Mitchell and by the National Institute of Aging.

The researchers reported having no conflicts of interest to disclose.

Primary source: Journal of Alzheimer's Disease
Source reference:
Mielke MM, et al "Plasma sphingomyelins are associated with cognitive progression in Alzheimer's disease" J Alzheimers Dis 2011; DOI: 10.3233/JAD-2011-110405.

Study: Apparent cause of accelerated formation of amyloid beta in Alzheimer's disease

2011-10-27T11:59:00.001-04:00

Here is a great dementia resource for caregivers and healthcare professinals,

Here is information on being the best caregiver you can be

Here is a way for nurses administrators, social workers and other health care professionals to get an easyceu or two

Follow Alzheimers1 on twitter

Cell Press

In their study, first author Dr. Markus P. Kummer and colleagues discovered that amyloid beta(AΒ) is a novel nitric oxide(NO) target. They observed nitrated AΒ in Alzheimer's disease(AD) and AD mouse models and found that this modification accelerated the deposition of human AΒ. Importantly, reduction of nitric oxide synthase(NOS2) reduced AΒ deposition and memory deficits in a mouse model of AD. Further, nitrated AΒ induced the formation of amyloid plaques when injected into the brains of mice with genetic mutations associated with AD.

"Taken together, our results identify a novel modification of AΒ, tyrosine nitration, and propose a causative link between the AΒ cascade, activation of NOS2, and the subsequent increase in its reaction product nitric oxide during AD," concludes Dr. Heneka. "We think that nitrated AΒ may serve as marker of early AΒ plaque formation. More importantly, it may be a promising target for an AD therapy, and that application of specific inhibitors of NOS2 may therefore open a new therapeutic avenue in AD."

Could taking vitamin C help those with dementia

2011-10-25T07:24:00.000-04:00

Here is a great dementia resource for caregivers and healthcare professinals,

Here is information on being the best caregiver you can be

Here is a way for nurses administrators, social workers and other health care professionals to get an easyceu or two

Times of India

Taking vitamin C might help patients with Alzheimer's disease, a study has suggested.

According to Lund University researchers, treatment with vitamin C can dissolve the toxic protein aggregates that build up in the brain in Alzheimer's disease.

The brains of people with Alzheimer's disease contain lumps of so-called amyloid plaques, which consist of misfolded protein aggregates. They cause nerve cell death in the brain and the first nerves to be attacked are the ones in the brain's memory centre.

"When we treated brain tissue from mice suffering from Alzheimer's disease with vitamin C, we could see that the toxic protein aggregates were dissolved. Our results show a previously unknown model for how vitamin C affects the amyloid plaques", said Katrin Mani, reader in Molecular Medicine at Lund University.

"Another interesting finding is that the useful vitamin C does not need to come from fresh fruit. In our experiments, we show that the vitamin C can also be absorbed in larger quantities in the form of dehydroascorbic acid from juice that has been kept overnight in a refrigerator, for example," added Mani.

There is at present no treatment that cures Alzheimer's disease, but the research is aimed at treatments and methods to delay and alleviate the progression of the disease by addressing the symptoms.

"The notion that vitamin C can have a positive effect on Alzheimer's disease is controversial, but our results open up new opportunities for research into Alzheimer's and the possibilities offered by vitamin C", said Mani.

The findings have been published in the Journal of Biological Chemistry .

Cognitive, Not Bio, Markers Predictive of Cognitive Decline

2011-10-23T06:06:00.001-04:00

Here is a great dementia resource for caregivers and healthcare professinals,

Here is information on being the best caregiver you can be

Here is a way for nurses administrators, social workers and other health care professionals to get an easyceu or two

Doctors Lounge

Cognitive markers are more effective predictors of conversion from mild cognitive impairment to Alzheimer's disease than biomarkers, according to a study published in the September issue of the Archives of General Psychiatry.

(HealthDay News) -- Cognitive markers are more effective predictors of conversion from mild cognitive impairment to Alzheimer's disease than biomarkers, according to a study published in the September issue of the Archives of General Psychiatry.

Jesus J. Gomar, Ph.D., from the Benito Menni Complex Assistencial en Salut Mental in Barcelona, Spain, and colleagues investigated the discriminative utility of different classes of biomarkers and cognitive markers by assessing their ability to predict conversion from mild cognitive impairment to Alzheimer's disease. The Alzheimer's Disease Neuroimaging Initiative (ADNI) database was analyzed to study 116 patients with mild cognitive impairment who converted to Alzheimer's disease, and 204 patients who did not convert within a two-year study period. The predictive utility of 25 variables from all classes of markers, biomarkers, and risk factors were determined by logistic regression models and effect size analyses.

The investigators found that, in logistic regression models, which included variables from all classes of markers, two measures of delayed verbal memory and middle temporal lobe cortical thickness predicted conversion within a two-year period. Effect size analyses revealed that biomarkers had modest change scores for two years, but change in an everyday functional activities measure was substantially larger. Approximately 50 percent of the predictive variance in conversion from mild cognitive impairment to Alzheimer's disease was attributed to decline in scores on the Functional Assessment Questionnaire and Trail Making Test, part B.

"We demonstrated that cognitive markers were consistently significant and generally stronger predictors than biomarkers," the authors write.

Two authors disclosed financial ties with the pharmaceutical industry. One of the study authors receives royalties for use of a cognitive test battery in clinical trials. The ADNI database used in the study was funded by the pharmaceutical industry.

Osteoarthritis accelerates and exacerbates Alzheimer's disease pathology in mice

2011-10-21T06:05:00.001-04:00

Here is a great dementia resource for caregivers and healthcare professinals,

Here is information on being the best caregiver you can be

Here is a way for nurses administrators, social workers and other health care professionals to get an easyceu or two

Journal of Neuroinflammation

tephanos Kyrkanides, Ross H Tallents, Jen-nie H Miller, Mallory E Olschowka, Renee Johnson, Meixiang Yang, John A Olschowka, Sabine M Brouxhon and M. KERRY O'Banion

Abstract (provisional)
Background
The purpose of this study was to investigate whether localized peripheral inflammation, such as osteoarthritis, contributes to neuroinflammation and neurodegenerative disease in vivo.

Method
S We employed the inducible Col1-IL1betaXAT mouse model of osteoarthritis, in which induction of osteoarthritis in the knees and temporomandibular joints resulted in astrocyte and microglial activation in the brain, accompanied by upregulation of inflammation-related gene expression. The biological significance of the link between peripheral and brain inflammation was explored in the APP/PS1 mouse model of Alzheimer's disease (AD) whereby osteoarthritis resulted in neuroinflammation as well as exacerbation and acceleration of AD pathology.

Results
Induction of osteoarthritis exacerbated and accelerated the development of neuroinflammation, as assessed by glial cell activation and quantification of inflammation-related mRNAs, as well as Abeta pathology, assessed by the number and size of amyloid plaques, in the APP/PS1; Col1-IL1betaXAT compound transgenic mouse.

Conclusion
This work supports a model by which peripheral inflammation triggers the development of neuroinflammation and subsequently the induction of AD pathology. Better understanding of the link between peripheral localized inflammation, whether in the form of osteoarthritis, atherosclerosis or other conditions, and brain inflammation, may prove critical to our understanding of the pathophysiology of disorders such as Alzheimer's, Parkinson's and other neurodegenerative diseases.

The complete article is available as a provisional PDF. The fully formatted PDF and HTML versions are in production.

Antiviral drugs could slow Alzheimer's disease

2011-10-19T04:34:00.000-04:00

Gantenerumab: New Alzheimer's drug shows early promise

2011-10-17T04:22:00.002-04:00

Here is a great dementia resource for caregivers and healthcare professinals,

Here is information on being the best caregiver you can be

Here is a way for nurses administrators, social workers and other health care professionals to get an easyceu or two

Follow Alzheimers1 on twitter

USA Today

The new study, which appears online Oct. 10 in the Archives of Neurology, is among the first to show the effects of an anti-amyloid drug in humans with Alzheimer's disease, but experts caution that while promising, more research is needed before this drug can be deemed safe or effective.
And, in what may turn out to be an equally important caveat, experts also say that it's by no means certain that reducing levels of amyloid plaque would stave off memory loss and the other mental declines associated with the disease because the role of the plaque in Alzheimer's isn't fully understood.
Alzheimer's disease is the most common form of dementia. Symptoms including serious memory loss, confusion and mood changes develop gradually and worsen with time. Recently, many strides have been made in diagnosing Alzheimer's disease earlier, but doctors have been stymied by a lack of effective treatments to stop or slow the course of the disease.
It's long been known that a protein fragment called beta-amyloid builds up in the spaces between nerve cells in the brains of people with Alzheimer's disease. The new drug, gantenerumab, targets these amyloid proteins by priming the body's immune system to recognize them as invaders.
Of 16 people with mild-to-moderate Alzheimer's disease, those who received two to seven infusions of the experimental drug every four weeks showed marked reductions in the amount of plaque in their brains via imaging tests that were conducted several months after their treatments.
By contrast, amyloid load increased among people who were randomized to receive the placebo. The new drug was given at either 60 or 200 milligrams (mg) doses. The higher dose yielded greater reductions in amyloid levels, the study showed. People who were given the 60 mg doses saw a nearly 16 percent reduction in the amount of amyloid, and those given the 200 mg doses saw a 36 percent reduction. The new study was conducted and funded by the drug's manufacturer, F. Hoffmann-LaRoche Ltd., in Basel, Switzerland.
The big question is whether or not reducing amyloid levels has any effect on the symptoms or progression of Alzheimer's disease, said Dr. Patrick Lyden, chief of neurology at Cedars-Sinai Medical Center in Los Angeles. "There is a growing concern that amyloid is a guilty bystander, but not the actual culprit in the brains of people with Alzheimer's disease, and taking away the bystander may not help the patient," he said.
There are approximately one dozen therapies, including vaccines, for Alzheimer's disease that are currently in the pipeline, Lyden noted. "They are all extremely exciting and promising in animals," he said. "This is the first one to show a preliminary result in people, but we have a huge way to go to make sure it is safe and improves symptoms."
Many in the Alzheimer's research community are awaiting these drugs with bated breath, but "none are ready for prime time," he said.
The leading theory of Alzheimer's disease is that an imbalance in the production or clearance of the amyloid plaque in the brain initiates a cascade of events that lead to dementia, explained Dr. Neelum Aggarwal, an associate professor of neurological sciences at Rush Alzheimer's Disease Research Center at Rush University Medical Center in Chicago.
"Accumulation of the plaques cause a variety of cellular responses: inflammation, neuronal death, and thus any potential treatment that can alter these processes would be beneficial," she said. The hope is that gantenerumab or other drugs like it will not only prevent amyloid from accumulating in the brain, but also slow down the cognitive impairment that occurs in people with Alzheimer's disease, she added.
That said, these experimental drugs carry the potential for serious side effects, including causing the immune system to go haywire. "The main issue that remains for this type of drug development is managing the immune response," Aggarwal said. Other side effects include a potentially fatal fluid build-up in certain areas of the brain. "This is problematic in that use of these treatments may carry a very high risk for neurologic complications, thus necessitating heightened monitoring, and diminishing its applicability as a treatment for a larger patient population such as the Alzheimer's disease population," she said.
If any of these drugs make it through the pipeline, it also needs to be determined who will get them, including whether the drugs will be given to prevent Alzheimer's in patients at high-risk of the disease or to treat it once it's started.
The need for a drug to delay the onset or slow progression of Alzheimer's disease can't be underestimated, Aggrawal said. In the United States alone, there are 5.4 million people with Alzheimer's disease, and the numbers are expected to increase to 13 million by 2050, when approximately three of every five people over the age of 85 will have Alzheimer's disease, she said.

Afib increases risk of dementia (part 2)

2011-10-15T04:35:00.000-04:00

Here is a great dementia resource for caregivers and healthcare professinals,

Here is information on being the best caregiver you can be

Here is a way for nurses administrators, social workers and other health care professionals to get an easyceu or two

Group Health

Dr. Dublin's study, which ran from 1994 to 2008, followed 3,045 people. The researchers relied on Group Health's advanced electronic data systems to determine whether participants had atrial fibrillation. The cognitive function of all study participants was evaluated every two years with tests and interviews as part of ACT. Patients whose ACT tests indicated possible dementia had additional tests including physical, neurological, and psychological exams, and many also had brain scans. A panel of experts determined the correct diagnosis for patients with cognitive problems.

Atrial fibrillation affects 3 million Americans. Dr. Dublin says that some ways it might increase dementia risk are:

•weakening the heart's pumping ability, leading to less oxygen going to the brain;

•increasing the chance of tiny blood clots going to the brain, causing small, clinically undetected strokes;

•a combination of these plus other factors that contribute to dementia such as inflammation.

Dr. Dublin said an important next step is studying whether any treatments for atrial fibrillation reduce the risk of developing dementia. The researchers also hope their results reach primary care providers, who are often the main doctors caring for people with atrial fibrillation, dementia, or both.

"Right now, we think we are protecting our patients' brains as long as they don't have a stroke, but tiny insults over time can add up," said Dr. Dublin, who is a primary care physician at Group Health. "This paper is a wakeup call, telling us that we need to learn more about how to protect brain function, while continuing to give patients with atrial fibrillation the best possible care."

Source: Group Health Research Institute

Lack of key protein linked to Alzheimer's

2011-10-13T05:53:00.011-04:00

Here is a great dementia resource for caregivers and healthcare professinals,

Here is information on being the best caregiver you can be

Here is a way for nurses administrators, social workers and other health care professionals to get an easyceu or two

Catholic Online (www.catholic.org)

Alzheimer's patients have lower levels of ubiquilin-1 in their brains, a study finds.

Scientists have found that Alzheimer's disease patients have reduced levels of a critical protein. The protein, ubiquilin-1, is found in nearly all tissues and is used by the body to mark damaged or unnecessary proteins for destruction. Reduced ubiquilin-1 means that other damaged proteins persist in the brain and contribute to the formation of cells that are associated with Alzheimer's.

LOS ANGELES, CA (Catholic Online) - The study observed for the first time, much lower than normal ubiquilin-1 levels in the entire set of 20 brains that were examined.

The lower levels means that other proteins, amyloid precursor proteins, which have been linked to Alzheimer's, are able to persist in the brains of patients instead of being properly regulated.

The information helps scientists to better understand the cause of Alzheimer's disease and may suggest new avenues for research and treatment.

Alzheimer's disease is a specific form of dementia that worsens over time and notoriously affects memory, thought, and behavior. It is also the most common form of dementia. Most patients are diagnosed as they grow older and find problems with language, decision-making and judgment.
Many simply attribute these symptoms to aging, but experts stress that such symptoms are not a normal part of the process. The rate of diagnosis of Alzheimer's is increasing, so scientists are anxious to learn more about the disease.

The link between ubiquilin-1 and Alzheimer's is new information for researchers.

The study was conducted by researchers at the University of Texas Medical branch at Galveston and published in the journal of Biological Chemistry.

What are those with dementia thinking

2011-10-11T07:22:00.000-04:00

Here is a great dementia resource for caregivers and healthcare professinals,

Here is information on being the best caregiver you can be

Here is a way for nurses administrators, social workers and other health care professionals to get an easyceu or two

Caring.com
Paula Spencer

In early/mid stages of Alzheimer's:

Most people are aware of initial cognitive changes in themselves (whether they say anything about it or not).
Self awareness doesn't disappear overnight. Research has shown that many people are relieved by a diagnosis of Alzheimer's, rather than upset, because they finally have a logical explanation for something unnerving that's dogged at them.

What helps: Taking action. Take expressed concerns about memory loss or other mental-functioning changes seriously. Recommend an evaluation, given that early interventions can help slow Alzheimer's progress. With someone already diagnosed, press the importance of making decisions regarding the future handling of health and legal affairs while the person is still able to express preferences.

The sense of self struggles to understand the changes, at first.
Some people try to explain it away: "I guess I'm getting old" or, "I never did have a good memory for detail." Some people willfully ignore changes, to the point where they don't seem bothered by them at all. Others actively and pragmatically work around failures of memory or cognition: They write notes, cede tasks that are too difficult, work crosswords or buy computer games to stimulate their brains.

What helps: Empathy and understanding. Don't pooh-pooh such observations. Look for ways to support the person's shortcomings: More clocks, a notebook in every room for keeping track of things, multiple pairs of sunglasses or tissue packs, or whatever seems to get misplaced often.

Awareness of the dementia effects can come and go.

The person may seem quite out of it, but the next be more engaged and "like his old self." Sometimes he used to catch himself, as if he realized this was the fifth retelling of an anecdote (though then he'd tell it anyway!).

What helps: Knowing these fluctuations are normal. Just because the person had clarity one moment, doesn't mean it will persist. Although the disease is progressive, it brings good days and bad days, a graph that would look more bumpy than slanted down a bit more each day.

In later stages of Alzheimer's:
The person is often or always oblivious to their condition.

The excuses or justifications fade away as self awareness fades. This can be a dangerous thing (as in the person who continues driving) or a blessing (as in the case of someone like my dad, who would be far more distressed about the extent of his condition if he were conscious of it)
What helps: Trust your gut. If the person seems content and uncomplaining, he or she may indeed be content, living in the moment. If the person is oblivious to the dementia but a threat to himself or others, you can't wait for clarity to kick in; you have to take action.

Emotional responses flatten or become misplaced – but remain.

I blogged recently about the amazing strength and importance of emotions in those who suffer with Alzheimer's, even for people deep into the disease process. You don't have to be aware of your limitations to be depressed or frustrated by them.

What helps: Physical contact. Touch is a messenger of reassurance and love. Offer a hug. Touch the person on the back or knee before you speak to avoid alarming them. Advanced Alzheimer's patients often find it soothing to stroke a tactile stuffed animal or hold a blanket.
Social skills and inhibitions fade as the social self unravels.
As a growing child learns what's socially appropriate, he shows fewer problem behaviors, like stripping off clothes on a whim or saying whatever pops into one's head. For someone who has Alzheimer's or, in particular, frontotemporal dementia, the opposite occurs. The social self unravels. A sense of what's appropriate or other sensibilities one once believed disappear, causing the person to say or do things that distress (hypersexual behavior, accusations of stealing, etc).

What helps: An ongoing social life. Even when it gets trying because of social inappropriateness, maintaining a social life (visits with relatives, conversation, the companionship of a pet) is important. Many researchers believe social connections help slow the disease process. It's not a cure, obviously, but like hugs and understanding, it never hurts.

Vegetarianism: Does it lower the risk of developing Alzheimer's disease

2011-10-09T07:22:00.001-04:00

Here is a great dementia resource for caregivers and healthcare professinals,

Here is information on being the best caregiver you can be

Here is a way for nurses administrators, social workers and other health care professionals to get an easyceu or two

Celestial Healing
There are many mental illnesses and disease that are related to the consumption of meat. Take Alzheimer for example. According to the American Alzheimer Association, between 6 and 8% of the population over 60 has Alzheimer's disease, and the rate has been increasing steadily. Several scientific literatures have affirmed that Alzheimer correlates with the consumption of meat and dairy. A review of studies published in Preventive Magazine two years ago sheds important light on a central risk factor in Alzheimers -- high levels of a blood substance called homocysteine.

Homocysteine is an amino acid. Amino acids are the building blocks of proteins. The only source of homocysteine for use in our bodies is that which the liver forms after the ingestion of another amino acid. Methionine is found in protein foods. Animal protein contains two to three times the amount of methionine as does plant protein. Homocysteine levels can be lowered very effectively by avoiding meat and dairy consumption. In fact, a recent study performed at Harvard Medical School showed that subjects who adopted a vegan diet had their homocysteine levels drop between 13% and 20% in just one week.

A 1993 study found that subjects, who ate meat, including poultry and fish, were more than twice as likely to become demented as their vegetarian counterparts. [Neuroepidemiology, 12:28-36, 1993]

Depression, anxiety, and schizophrenia can be connected to meat consumption. The amount of tryptophan (An amino acid necessary for normal growth in infants and for nitrogen balance in adults.) in the foods that are eaten has only a small influence upon the amount of tryptophan that enters the brain. The most important factor determining the total amount of tryptophan that does enter the brain is the concentration of other large-molecule amino acids concurrently present in the blood. Large-molecule amino acids, among them tryptophan, compete with each other to enter "gates" between the circulating blood stream and the relatively confined brain fluids. A high-protein meal (full of meats, dairy foods, and eggs) provides many other amino acids that compete with tryptophan for entry into the brain; the end result is less tryptophan passing into the brain and a decrease in the synthesis of serotonin (a phenolic amine neurotransmitter that is a powerful vasoconstrictor and is found especially in the brain, blood serum, and gastric mucosa of mammals). Conversely, a low-protein, carbohydrate-rich diet (full of starches, vegetables, and fruits) results in the highest levels of serotonin in the brain, because fewer large-molecule amino acids are competing with tryptophan to enter the brain. For most this means less hyperactivity, anxiety, depression, and insomnia-provided they eat a vegetarian diet.

In some people anxiety, depression, and fatigue are caused by allergic reactions to foods. The most common causes of food allergies are dairy products, followed by eggs. These reactions are often subtle and difficult to recognize until the offending food has been eliminated, either by accident or by intention, and then, later, when the body is challenged with the suspect food, a recognizably adverse reaction occurs.
A serious psychological disease caused by foods in some people is schizophrenia. In hospital-based studies, some patients have been identified who react with dramatic behavioral changes to milk products and animal products. Some people with schizophrenia have actually been cured of their disease by changing their diet, (eliminating meat and dairy) and including more natural foods like fruits, vegetables, and whole grains.

I recall an Herbalist saying, “Tell me what a person eats and I shall tell you what sort of person he or she is and what type of character and behavior they hold.” No doubt, there are other factors also that determine a person's personality and behavior, but food also has a great effect on one's mind. Experience tells me that one's diet is closely connected with one's thoughts and conduct. So anyone who wishes to purify their thoughts and to elevate their character must partake in a vegetarian diet. If we eat live food, we will be helping our mind and emotions to remain in a state of peace and self-control. Pure food enables one to feel light and fresh and the mind opens out to the pure life and beauty of the world. The mind becomes undisciplined, wild, agitated or fickle when the diet is exciting, intoxicating or inebriating (intoxicant), the character constantly declines and the result is tension, depression, sorrow and disquiet.
Finally, the subject of meat consumption linked to brain disease has firmly come to the front of my research with the issue of “mad cow” disease. While scientist debate whether it is due to a mysterious prion or a virus, health-conscious advocates and nutritionist are using the scandal to point out numerous disadvantages of the typical animal-based Western diet as well as the corrupt manner in which the meat-producing industry is manufacturing its products. Specifically, it is imagined that ‘mad cow’ disease results from contaminated animal feed which has been fortified with ground up intestines, brains, spinal cords, bones, and other parts from cows, chickens and sheep – in effect turning herbivores into cannibalistic carnivores. Four with “mad cow” disease (also known as bovine spongiform encephalopathy – BSE), which is being linked to a correspondingly similar brain disorder in humans known as Creutzfeldt-Jakob disease, the symptoms are attributed to microscopic holes in the brain. So how did cows get mad cow disease, known by its medical name as "bovine spongiform encephalopathy," or "BSE"? For several decades, cattle feed had included a cheap protein supplement made from the carcasses of other animals, including sheep and cows. BSE probably arose when sheep infected with scrapie or cows with BSE were turned into feed. The feed then infected other cows that ate it, and when those animals died, they were fed back to more cows, creating a rapidly escalating epidemic. It was a kind of cattle cannibalism. And for two years after BSE was known, infected cattle were still allowed into England's food supply, raising fears that people might get BSE. To assess that risk, the British government called upon the scientific community. The scientific community noticed several behaviors, which has been related to the effects of people who ate beef from cows with “mad cows” disease. Some of those behaviors were hallucination, disorderly conduct, hyperactivity rudeness, agitation, and neglectfulness. With all this information, I see why Oprah stated to millions of Americans that she will never eat another hamburger again.

A vegetarian diet produces higher levels of behavior than a diet containing meat when all types of caloric intake are equal. Vegetarians were shown in one university study to score higher on examinations than meat eaters. Vegetarians also showed less frustration and lower levels of irascibility than meat eaters. (Bulletin of the Psychosomatic Society 10:35-36, July 1977)

Vegetarianism is a cause that addresses several key major social issues: ethics, the environment, and health – mental, spiritual and emotional as well as physical. As Albert Einstein wrote: "Nothing will benefit human health or increase the chances for survival of life on earth as the evolution to a vegetarian diet. It is my view that the vegetarian manner of living, by its purely physical effect on the human temperament, would most beneficially influence the lot of mankind."

The correlation between people who eat meat and violence

Managing mealtime tasks: told by persons with dementia

2011-10-07T02:17:00.001-04:00

Here is a great dementia resource for caregivers and healthcare professinals,

Here is information on being the best caregiver you can be

Here is a way for nurses administrators, social workers and other health care professionals to get an easyceu or two

Journal of Clinical Nursing
Linda Johansson,, Lennart Christensson,, Birgitta Sidenvall

Aim. To capture the self-description of managing mealtime tasks by persons with dementia.

Background. There are several factors that negatively affect food intake in persons with dementia that may increase the risk of developing malnutrition. Difficulties in managing daily activities increase gradually and mealtime tasks like food shopping, cooking and eating often become troublesome. Still, little is known about how persons with dementia themselves experience this issue.

Design. A qualitative study with an ethnographic approach.

Method. Ten women and five men aged 69–86 with dementia were interviewed. Interviews were carried out in the informants’ own homes and a thematic analysis was performed.

Results. The informants described that they wanted to be independent and that the memory loss was not affecting them to a great extent. Old habits and routines, as well as newly developed strategies, helped them manage mealtime tasks despite the disease. Informants were satisfied with their current situation, even though it sometimes meant that they had changed their way of managing mealtime tasks, for instance receiving meals-on-wheels.

Conclusions. Persons with dementia seem to be able to manage mealtime tasks and these activities were based on old habits and routines. Independence was highly valued and managing mealtime tasks seems to be one way to appear independent.

Relevance to clinical practice. It is important for caregivers to understand that persons with dementia might not express difficulties in managing mealtime tasks for fear of losing their independence. It is, therefore, important to create a trustful relationship even before problems arise to be able to support the persons when necessary

View Full Article (HTML) Get PDF (109K)

Can veggie juice lower risk of Alzheimer's?

2011-10-05T02:24:00.001-04:00

Common Signs of Aging Traced to Tiny Brain Blockages

2011-10-03T01:30:00.000-04:00

Here is a great dementia resource for caregivers and healthcare professinals,

Here is information on being the best caregiver you can be

Here is a way for nurses administrators, social workers and other health care professionals to get an easyceu or two

By John Gever, Senior Editor, MedPage Today

Blocked blood vessels in the brain, often too small to be seen with current medical imaging technologies, may explain some of the common signs of aging such as diminished walking ability and hand tremors, researchers said.

Brain autopsy findings showed microscopic infarcts in 57 individuals out of 418 examined, the presence of which was significantly associated with gait abnormalities similar to those seen in Parkinson's disease, reported Aron S. Buchman, MD, of Rush University in Chicago, and colleagues.
Signs of arteriolosclerosis invisible with standard imaging were also significantly associated witparkinsonian gait, as were macroscopic infarcts that would be picked up with CT or MRI scans, the researchers indicated online in Stroke: Journal of the American Heart Association.

"We are not aware of previous studies demonstrating independent roles for microinfarcts and the severity of arteriolosclerosis in the development of parkinsonian gait," Buchman and colleagues wrote.

"Given that microinfarcts and severity of arteriolosclerosis are not discernible during life, these pathologies likely represent unrecognized common etiologies for parkinsonian gait in older persons and support clinical-imaging studies that suggest subclinical cerebrovascular disease abnormalities are associated with gait dysfunction in older persons."

The researchers added that more aggressive prevention and treatment strategies for vascular risk factors "might decrease the burden of mild age-related parkinsonian signs."

Such symptoms, which include rigidity and sluggish movements as well as tremors and gait problems -- are common in the elderly, affecting up to half of noninstitutionalized people 85 and older, according to Buchman and colleagues.

They pointed out that, although these symptoms are shared with Parkinson's disease (hence the "parkinsonian" rubric), most individuals showing them do not have the disease, as Lewy bodies and nigral degeneration, its neurological hallmarks, are absent.

On the other hand, cerebrovascular defects are common in older people and are known to produce parkinsonian symptoms, the researchers indicated.

To explore the connection, they reviewed autopsy findings from 418 deceased participants in the Rush Religous Orders Study, a prospective study that began in 1993 involving some 1,100 older nuns, brothers, and priests who underwent annual physical and psychological exams.

Those included in the current analysis had no signs of dementia at enrollment. At death, they averaged 88.5 years old and about 60% were women. Mean scores on the Mini-Mental State Examination at their last visit were 22.7, indicating significant cognitive impairment.

Microscopic infarcts were present without other abnormalities in 7.9%, and accompanied by arteriolosclerosis not detected in brain scans in 5.7%.

These small arteriolosclerosis lesions were seen alone in 14.8% of the autopsied brains, and relatively large infarcts were found in 36%.

At their yearly evaluations, study enrollees were assessed for Parkinsonian symptoms using a 26-item instrument derived from the Unified Parkinson's Disease Rating Scale. Each of the four major symptoms -- abnormal gait, bradykinesia, tremor, and rigidity -- were evaluated on 100-point scales. The average of these scores served as a global summary.

At death, the 418 individuals had had the following mean scores at their last evaluation:

•Gait: 41.5

•Rigidity: 11.7

•Bradykinesia: 21.4

•Tremor: 5.2

•Global summary: 18.6

Macroscopic infarcts were the most powerful predictors of these symptoms. Their presence was associated with increases of 0.359 points in the global score (P=0.013), 0.552 points on the gait scale (P=0.009), and 0.853 points on the rigidity scale (P<0.001).

Infarcts too small to be seen on imaging were associated with a 0.424-point increase in gait scores (P=0.047).

Arteriolosclerosis was a much smaller factor, although its association with gait scores (0.191 points, P<0.001) was statistically significant.

The location of infarcts within the brain appeared partly to determine their impact on parkinsonian signs. Multiple subcortical microinfarcts were more strongly associated with impaired gait (0.888 points, P=0.004) than cortical microinfarcts, the researchers found.

Similarly, subcortical macroscopic infarcts were also apparently more damaging than those within the cortex.

"Together these data suggest that a substantial portion of older people have brain tissue damage and small vessel disease that are unlikely to be detected before death and suggest that cerebrovascular disease may be an even larger public health challenge than currently estimated," Buchman and colleagues wrote.

They cited some limitations to the study. Microinfarcts and small arteriolosclerosis lesions were counted only in certain brain regions, potentially underestimating the association with parkinsonian signs. Study participants did not undergo brain imaging, so it is possible that signs of the cerebrovascular defects could be discernible in some cases.

Finally, the cross-sectional study design precludes firm conclusions about the direction of causality.

"It is possible that the cerebrovascular pathologies do not play a causal role in the development of parkinsonian signs, but rather both cerebrovascular pathologies and parkinsonian signs might be caused by a third factor," Buchman and colleagues noted.

The analysis was supported by the National Institutes of Health and the Illinois Department of Public Health.

Study authors declared they had no relevant financial interests.

Primary source: Stroke

Source reference:

Buchman A, et al "Cerebrovascular disease pathology and parkinsonian signs in old age" Stroke 2011; DOI: 10.1161/STROKEAHA.111.623462.

Is Alzheimer|s preventable?

2011-10-01T04:34:00.000-04:00

Alzheimer's disease looks different in people over 80

2011-09-29T04:33:00.000-04:00

Sophisticated scan may spot seeds of Alzheimer's risk

2011-09-27T07:23:00.001-04:00

Calcified Plaque in Arteries May Pose Stroke, Dementia Risk

2011-09-25T02:25:00.002-04:00

Atypical psychotics may hasten dementia decline (part 2)

2011-09-23T02:26:00.001-04:00

Here is a great dementia resource for caregivers and healthcare professinals,

Here is information on being the best caregiver you can be

Here is a way for nurses administrators, social workers and other health care professionals to get an easyceu or two

Medscape Today
Deborah Brauser

great deal of care," said Dr. Schneider.

He added that the meta-analysis showing a link between atypical antipsychotics and increased mortality risk in an elderly population with dementia helped support the Food and Drug Administration's (FDA's) subsequent black box warning in 2005.

A recent study published in the Archives of General Psychiatry and reported by Medscape Medical News at that timeshowed use of atypicals to treat behavioral symptoms has decreased significantly since the FDA warning was issued. However, other studies have shown that the overall prescription rate has not decreased ( Arch Intern Med. 2010;170:89-95 and CMAJ. 2008;179:438-446).

In the current study, investigators evaluated data on the 421 outpatients with AD and psychosis or aggressive behavior from CATIE-AD, which was conducted at 45 sites in the United States between April 2001 and November 2004.

Significant Decline

During the first phase of the trial all participants were randomized to receive flexible doses of either olanzapine (n = 100; mean dose, 5.5 mg/day), quetiapine (n = 94; mean dose, 56.5 mg/day), risperidone (n = 85; mean dose, 1.0 mg/day), or placebo (n = 142).

After 2 weeks, they could discontinue their allocated treatment and switch to another randomly assigned medication, on their clinicians' request. If they discontinued use of that medication, patients could move into phase 3 of the study, which consisted of open-label treatment with one of the other randomly assigned study drugs.

"At any time, the clinician could choose to enter the patient into phase 4, where data collection continued but the physician prescribed medication," explain the researchers.

The subjects were followed up for 9 months and scheduled to undergo cognitive assessments at the 12-, 24-, and 36-week timepoints. This new analysis assessed the 357 patients (54% male; mean age, 77.6 years) who participated in at least 1 baseline and 1 follow-up cognitive measure.

Measurements included the Mini-Mental State Examination (MMSE), the cognitive subscales of the AD Assessment Scale (ADAS-Cog) and of the Brief Psychiatric Rating Scale (BPRS), a cognitive summary score that combined changes on 18 cognitive tests, and the Clinical Global Impression of Change (CGIC).

Results showed that at 36-week follow-up all of the patients had declined significantly in most cognitive areas, including worsening scores on the MMSE (−2.4 points) and ADAS-Cog (−4.4 points).

The only statistically significant difference between individual antipsychotic groups and the placebo group were greater cognitive decline in the following:

•the cognition summary for those taking olanzapine or risperidone (P = .04 and P = .001, respectively);
•the MMSE for those taking olanzapine (P = .05); and
•BPRS for those taking quetiapine (P = .05).
When all 3 atypical groups were combined, participants' cognitive function decreased significantly more than their counterparts who were taking placebo on the MMSE (P = .004), BPRS (P = .05), and cognitive summary (P = .004).

"Over the 36-week trial period, patients receiving any antipsychotic had an average decline 2.46 points greater on the MMSE than placebo patients, a difference both statistically significant and clinically relevant," write the researchers.

The average CGIC scores for all 4 groups indicated minimal improvement and did not differ significantly (placebo, 3.13; olanzapine, 3.11; quetiapine, 2.83; risperidone, 2.81).

Permanent Effect?

"Because we did not measure differences in the rates of cognitive decline over longer exposure periods, we cannot address the question of whether these drugs would accelerate [the] decline permanently or merely impair cognition during acute administration," the investigators write.

They note that they also do not know whether the decrease in cognition was due to a worsening of Alzheimer's pathology or if it was an independent effect.

Much of medication use is due to the lack of interest, willingness, funding, or ability to provide psychosocial or environmental interventions to patients with agitation, aggression, and psychosis who have dementia.
Although the investigators write that the declines found in this study reached "at least as great a magnitude as the effect of cholinesterase inhibitors but in the negative direction," they add that use of atypicals may still be warranted in individual cases.

"The relative adverse effects on cognitive function within the class of medication need to be addressed in further studies that include assessment of attention, psychomotor function, and executive function," they write.

Dr. Schneider noted that nonpharmacologic treatments should also be investigated.

"Much of medication use is due to the lack of interest, willingness, funding, or ability to provide psychosocial or environmental interventions to patients with agitation, aggression, and psychosis who have dementia."

He explained that much agitation can be redirected and that aggression often comes about due to cognitive impairment — and can be mitigated by the way caregivers react to or communicate with patients.

"These approaches have limits too, but certainly they are not applied enough because they involve significant amounts of time and training," said Dr. Schneider.

Few Alternative Treatments

"Risk-benefit analysis is always part of the decision to use psychotropic medication. The aged are a particularly vulnerable group, and this study strongly underscores that vulnerability," write D. P. Devanand, MD, from the Division of Geriatric Psychiatry at the College of Physicians and Surgeons at Columbia University in New York City, and Susan K. Schultz, MD, from the Department of Psychiatry at the University of Iowa College of Medicine in Iowa City, in an accompanying editorial.

"Neuropsychological testing across a range of domains in this study offers a powerful look at the progression of AD in the context of treating neuropsychiatric symptoms," they add.

However, they caution that several caveats should be considered "when interpreting the findings and their potential impact on clinical practice," including that the investigators had to combine the 3 treatment groups to find statistical differences from placebo on the MMSE and the summary scores.

"It is likely that individual vulnerabilities to specific antipsychotics are mediated by a variety of factors, including concomitant medications, medical comorbidity, and underlying frailty, that are beyond the scope of this analysis."

Despite the widespread awareness of adverse consequences, we can only infer that atypical antipsychotics continue to be prescribed for dementia treatment because there is a lack of alternatives and there is a perceived clinical benefit by care providers.
In addition, the editorialists note that "while dose effects were not addressed in this analysis, adverse events in this population are dose related, and treatment dropouts occur more frequently with risperidone doses above 2 mg and olanzapine doses above 5 mg."

Other concerns cited include that data for any patient receiving an antipsychotic for at least 2 weeks was included, whether they had switched medications or not, which may result in short-term harmful effects that may not continue with longer treatment exposure.

Dr. Devanand and Dr. Schultz note that alternative pharmacologic treatments, such as benzodiazepines, also provide risky cognitive liabilities.

"Despite the widespread awareness of adverse consequences, we can only infer that atypical antipsychotics continue to be prescribed for dementia treatment because there is a lack of alternatives and there is a perceived clinical benefit by care providers," they write.

"These complex issues will require a thoughtful and balanced evaluation with an appreciation of the care setting, individual patient vulnerabilities, and goals of care."

The study was supported by the National Institute of Mental Health, the USC Alzheimer's Disease Research Center, and the Department of Veterans Affairs. Medications were provided by AstraZeneca, Forest, Janssen, and Eli Lilly. The study authors report several disclosures, which are listed in the original article. The editorialists report having received research support from Eli Lilly and Novartis and are currently consultants for Bristol-Myers Squibb and Sanofi-Aventis.

Atypical antipsychotic drugs may hasten dementia decline

2011-09-21T02:29:00.002-04:00

New way for treating Alzheimer's disease

2011-09-19T06:04:00.001-04:00

Here is a great dementia resource for caregivers and healthcare professinals,

Here is information on being the best caregiver you can be

Here is a way for nurses administrators, social workers and other health care professionals to get an easyceu or two

Follow Alzheimers1 on twitter

Examiner.com
Ruben Dagda, Pittsburgh Medical Technology Examiner

Making the blood brain barrier more permeable may be the answer

Although there is currently no cure for treating Parkinson's and Alzheimer's disease, a preclinical study published yesterday at the prestigious Journal of Neuroscience may revolutionize the way patients will be treated in the US. Currently, one of the major impediments for treating many neurodegenerative diseases is the fact that the blood brain barrier is highly impermeable to most FDA approved and experimental drugs. Therefore, only a small fraction of the drug reaches the brain and has a therapeutic effect.

However, scientists from Cornell University discovered a way to make the blood brain barrier more permeable so that the brain absorbs a higher amount of therapeutic drugs: by using adenosine agonists. In brief, scientists discovered that mice intravenously injected with drugs that stimulate adenosine receptors (NECA) were able to accumulate a higher amount of an experimental sugar molecule (dextran) in the brain upto three times more compared to untreated animals. The modified sugar stayed in the brain upto 24 hrs. following a single intravenous injection of the adenosine receptor agonist drug. The effect of the drugs on the blood brain barrier is specific for adenosine receptors since mice that lacked adenosine receptors did not accumulate the dextran in the brain.

What is the medical relevance of this study?

A pathological hallmark of Alzheimer's disease is that patients accumulate protein garbage in neurons called beta-amyloid and tau protein which is associated with the destruction of memory neurons. Using a mouse model of Alzheimer's disease, the scientists showed that mice co-injected with adenosine agonists and with beta amyloid busters (a monoclonal antibody called 6E10) were able to bind to beta amyloid deposits in mice. This experiment is a proof of principle for using drugs that can make the blood brain barrier and with FDA approved drugs for Alzheimer's disease such as acetycholinesterase inhibitors. This study is promising and can lead to the creation of new revolutionary therapies for treating Alzheimer's disease.

Final remarks-

Approximately about 5.5 million people are afflicted with Alzheimer's and Parkinson's disease in the US. Many patients over 65 years of age are relegated to spending their final days of life in nursing homes or are cared by family members which can be a great economic and emotional burden.

There is a great need for finding safe and efficient techniques to administer drugs that can penetrate the blood brain barrier in high concentrations. Nowadays, some patients undergo highly invasive techniques such as direct injections of drugs into the ventricles of the brain, epidural injections or installing intracranial pumps to treat neurodegenerative diseases. Also, most drugs need to be chemically modified so that it can reach the blood brain barrier but renders the drug also capable to concentrate in unwanted tissues.

But what if we can avoid all this hassle and inconvenience of undergoing painful surgical procedures or spending a high amount of money on drugs that do not reach the brain? For instance about less than 10% of Parkinson's disease drugs such as Levodopa in combination with Carbidopa reach the brain while the rest is metabolized and wasted in Parkinson's disease patients. The solution proposed by the authors could bring down the costs of anti-neurodegenerative drugs and increase patient compliance.

The only downside is that patients will not be able to drink coffee or other caffeinated products if adenosine analogues or the FDA approved Lexiscan is used as treatment for Parkinson's and Alzheimer's.

References:

Carman, A., Mills, J. Krenz, A., Kim, D. Bynoe, M. Adenosine receptor signaling modulates permeability of the blood-brain barrier, 2011, The Journal of Neuroscience 31(37): 13272-13280.

Did you find this article interesting? then share my article with friends, send me a comment or follow Alzheimers1 on twitter.

Intranasal insulin treatment for Alzheimer's disease

2011-09-17T06:04:00.001-04:00

Here is a great dementia resource for caregivers and healthcare professinals,

Here is information on being the best caregiver you can be

Here is a way for nurses administrators, social workers and other health care professionals to get an easyceu or two

Alzheimer's Association

Currently, there is no cure for Alzheimer's disease. But drug and non-drug treatments may help with both cognitive and behavioral symptoms. Researchers are looking for new treatments to alter the course of the disease and improve the quality of life for people with dementia.

In an article published September 13, 2011, in the Archives of Neurology, results from a small, short-term treatment trial (four months) of intranasal insulin in Alzheimer's disease and mild cognitive impairment (MCI) showed statistically significant benefits on certain tests of memory and functioning, but no changes on some others. In those people who showed benefits on memory tests, the researchers also measured changes in chemicals in participants' spinal fluid that may indicate a beneficial effect of the treatment on Alzheimer's.

It is important to note that, quite often, preliminary studies like this generate positive results but fail to show long-term benefit in larger trials. That said, these findings are very encouraging, and further research — longer trials with larger numbers of participants — of intranasal insulin as a therapy for Alzheimer's and MCI is warranted.

We urgently need earlier detection and better treatments for Alzheimer's, which is a devastating, heartbreaking and fatal disease, and a growing epidemic. This requires a greater commitment to research — increasing funding for Alzheimer's research and recruiting more volunteers for Alzheimer's clinical trials.

Researchers selected 104 men and women for the study. All had either mild to moderate Alzheimer's or mild cognitive impairment, a condition that increases the risk of developing Alzheimer's, especially when memory is affected. The participants were divided into three groups. Using a nasal spray, each group received twice-daily doses of either lower or higher doses of insulin or a placebo.

The study found that men and women who used the lower dose of insulin nasal spray tended to score better on memory tests than those who used the placebo. No improvement was seen in those receiving the higher insulin dose. Both groups receiving insulin preserved their level of daily functioning, according to reports from their caregivers, while participants in the placebo group showed an overall decline in function. Few side effects occurred among those treated with the insulin spray, other than occasional light-headedness and dizziness or stuffy nose.

Related
•Minor ailments linked to Alzheimer's. Read
•Can you walk away from dementia? Read
•Eating berries may protect against dementia, Alzheimer's. Read
•Do drugs for treating early-stage Alzheimer's work? Read

The brain needs insulin

Over the past 10 years scientists have come to learn that insulin plays an important role in the brain, says clinical neuroscientist Suzanne Craft, of the Veterans Affairs Puget Sound Health Care System and the University of Washington School of Medicine. It helps the brain form memories, allows brain cells to communicate with one another and manages levels of brain chemicals.

All cells, including those that make up the brain, use glucose for energy. The hormone insulin makes it possible for glucose, aka blood sugar, to enter cells, enabling them to work properly. With age, however, many people develop a problem called insulin resistance, a condition in which the body and the brain do not use insulin effectively.

If glucose cannot enter brain cells, the cells won't carry out their tasks related to memory and thinking. "This sets the stage for problems in brain function that may develop into conditions like Alzheimer's disease," says Craft, lead author of the study. She and her colleagues set out to determine whether providing insulin directly to the brain could improve the cell's ability to use insulin.

Top ways to celebrate Rosh Hashanah with those who have dementia

2011-09-15T05:39:00.003-04:00

Why you should celebrate World Alzheimer's Day on September 21

2011-09-13T07:32:00.001-04:00

World Alzheimer's Day

Caregivers, and healthcare professionals,here is interesting information
Here is a great dementia resource for caregivers and healthcare professinals,

Here is information on being the best caregiver you can be

Here are more interesting dementia brain boosting activities

Healthnews-stat.com

Author Susan Berg says "It is everyone’s duty to embrace this day because there is no time to lose when fighting the battle of preventing this terrible disease." Here are some simple things you can do

What do you know about Alzheimer’s disease and related dementias?

How can you decrease your chances of getting these disease?

How can you help someone with Alzheimer’s disease or a related dementia?

This year’s theme is 'Faces of dementia'
'
Yes, there is an urgency for all to learn about these diseases and do what they can to prevent them in themselves. Also legislators need to contacted so more funds can be allocated for research. World Alzheimer’s day, on Sept 21, is the perfect time to do this.

Approximately 5.5 million people in the United States already have Alzheimer’s disease or a related dementia. The number will continue to grow as the baby boomers reach the age of retirement.

What can you do right now to lessen your chances of getting these diseases?

1. Stop smoking! There is nothing positive about smoking. Studies have shown that smoking not only raises your chances of developing dementia, but it also increases your chances of getting other diseases.

2. Eat a healthy diet. Research suggests that the Mediterranean diet staves off the onset of dementia

3. Keep mentally active. Again studies have shown this, to be a way to delay the onset of dementia.

4. Keep physically active. Research indicates that moderate exercise at least a half an hour three times a week is another way to keep dementia from affecting you.

How can you help others?

Donate to the Alzheimer’s Association. Give your time and/ or money. Help with special events. Organize fund raisers.

Susan Berg has written a book called, Adorable Photographs of Our Baby, for those with dementia, their caregivers, and interested professionals.
She is donating money to the Alzheimer’s Association for each book she sells. She is passionate about educating others on these diseases. Visit her blog at http://dementiaviews.blogspot.com.

You or someone you know could develop symptoms tomorrow. The cost of caring for those with Alzheimer’s disease or a related dementia is expensive monetarily, physically, emotionally, and psychologically.

So please acknowledge World Alzheimer’s Day, this Tuesday, September 21

Heart's Pumping Ability May Hold Key to Dementia

2011-09-11T08:04:00.001-04:00

Here is a great dementia resource for caregivers and healthcare professinals,

Here is information on being the best caregiver you can be

Here is a way for nurses administrators, social workers and other health care professionals to get an easyceu or two

By Kristina Fiore, Staff Writer, MedPage Today
Reviewed by Robert Jasmer, MD; Associate Clinical Professor of Medicine, University of California, San Francisco and
Dorothy Caputo, MA, RN, BC-ADM, CDE, Nurse Planner

Left ventricular ejection fraction (LVEF) may play a role in cognitive aging, but that role is not a simple matter of impaired LVEF, researchers found.

Patients in lowest quartile of LVEF performed significantly worse on several cognitive tests than patients in middle quintiles, but there was no linear association since U-shaped curves also showing an association between the highest LVEF levels and cognitive aging, Angela Jefferson, PhD, of Boston University, and colleagues reported online in the American Journal of Cardiology.

Jefferson and colleagues called these findings "unexpected."

Heart failure is a known risk factor for Alzheimer's disease and cerebrovascular disease. But even in the absence of end-stage heart disease, it's thought that LVEF may have an affect on brain aging.

To test their hypothesis that lower LVEF was associated with cognitive and neuroimaging markers of preclinical Alzheimer's disease, Jefferson and colleagues looked at data from the Framingham Offspring Study, an offshoot of the Heart study.

They analyzed brain MRI and cardiac MRI studies as well as the results of neuropsychological examinations for 1,114 patients -- mean age 67 -- who didn't have stroke or dementia.

Multivariate analyses revealed overall that LVEF wasn't associated with any brain variable.

However, there were several U-shaped associations when LVEF levels were separated into quintiles.

Patients in the first quintile, or those with the lowest LVEF values, had lower mean cognitive performance on several cognitive tests, including the Visual Reproduction Delayed Recall and the Hooper Visual Organization Test, compared with patients in the middle quintiles (P<0.001 for both).

But the researchers noted that there were no differences among groups on any of the brain MRI variables.

Unexpectedly, they said, patients in the highest quintile of LVEF values also had lower mean performance on cognitive tests, including the Logical Memory Delayed Recall (P=0.03), the Visual Reproduction Delayed Recall (P=0.03), the Trail Making Test (P=0.02), and the Hooper Visual Organization Test (P=0.02).

Jefferson and colleagues reported that the associations were similar even after excluding prevalent cardiovascular disease.

"The observation that a lower LVEF is associated with abnormal brain changes extends previous research examining patients with severe cardiomyopathies, which reported that a reduced LVEF was associated with memory, reasoning, and sequencing impairments," they wrote.

"While healthy LVEFs may be good for brain health, very high LVEFs may correspond to subtle cognitive impairment," they wrote, adding that the finding may also be a sign of another pathologic process such as anemia or thyroid disease.

The study was limited by its use of observational, cross-sectional data, which cannot establish causality. The study may also be limited in generalizability, because the cohort was predominantly white and middle-aged to elderly.

Still, they concluded that "in the absence of clinical heart failure and prevalent cardiovascular disease, our findings suggest that lower LVEFs are also related to abnormal brain aging."

The danger of your aging parent covering up dementia (part 2)

2011-09-09T07:26:00.001-04:00

Here is a great dementia resource for caregivers and healthcare professinals,

Here is information on being the best caregiver you can be

Here is a way for nurses administrators, social workers and other health care professionals to get an easyceu or two

Forbes

Carolyn Rosenblatt

Mom just steps in and does what Dad is forgetting. He forgot, for instance, how to make coffee. He’s been making coffee for decades. He forgot the steps. He didn’t remember them later. He got lost driving home. Is that “normal” because he’s 86? It isn’t. Both of these memory issues are signs of trouble brewing.

Dad refused to try a new card game, something he’s always loved to do in the past. He is having more and more trouble learning any new information, say nothing of keeping track of the information he already knows.

Jaclyn wants to help, but is afraid to bring up the subject of what she sees. Mom will just deny a problem and say Dad is fine, just getting old.

Does it matter whether Dad goes to see a neurologist? Yes. At least that can help sort out the behavior that is not what the family is used to seeing and rule out various causes. Medication interactions, infections, stroke, and even dehydration can cause changes in brain function and behavior. It’s good to find out possible reasons for the memory problems and learn whether they can be treated.

A doctor generally won’t diagnose Alzheimer’s Disease unless there is enough evidence from testing and examining a patient to give the physician reasons to do so. There’s no one test to tell you if your aging parent has it or not. We get clues and doctors draw reasonable conclusions from them, but it’s not a precise thing.

Regardless, if your aging parent is showing the signs Jaclyn’s father is showing, you can take better control of how you handle the problem by acting on the signs rather than ignoring them. You can be sure that if Dad gets lost driving home, his driving days should come to an end. That is definitely worth talking to the doctor about, as Dad may need help facing the enormous consequences of losing the ability to drive.

If there is no official diagnosis other than “early dementia” or “mild cognitive impairment”, it’s not a signal to the family that everything is ok and no one needs to plan ahead. Rather, it’s time to take a look at Dad’s future. In advising Jaclyn, I gave her a list of a few things to check into now, rather than wait for a crisis.

Here’s Jaclyn’s 4-item beginning “to do” list:

The Danger Of Your Aging Parent Covering Up Dementia

2011-09-07T04:33:00.004-04:00