Framework of the National Alzheimer's Plan is only the beginning

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

Alzheimer's Association

The efforts and input of the Alzheimer's Association and our advocates were crucial to the passage of the National Alzheimer's Project Act (NAPA) and its upcoming implementation as the National Alzheimer's Plan. We still have much work ahead to ensure we build on the momentum to lead our country toward overcoming the Alzheimer's crisis. Lend your VOICE in the fight against Alzheimer's disease and attend the 2012 Alzheimer's Association Advocacy Forum, April 23-25, in Washington, D.C.

2012 Alzheimer's Association Advocacy Forum
Make your VOICE heard! Every story matters, every story counts.

Amplify your VOICE by joining us this year as we convene in our nation's capital on April 23-25, 2012 for the Alzheimer's Association Advocacy Forum.

Help build the national movement to end Alzheimer's by being educated about legislative issues; networking with advocates from across the nation to make our case loud and clear as we demonstrate the commitment to advancing our legislative agenda and a world without Alzheimer's disease.

Register Now

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

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

Mail Online

Cells damaged by Alzheimer's created for first time
Hoped discovery will enable better understanding of dementia

By SADIE WHITELOCKS

Brain cells damaged by Alzheimer's have been created for the first time, offering hope to dementia patients.
It is believe that the breakthrough could help scientists better understand how the degenerative condition affects the the nervous system, prompting more effective treatment.
Alzheimer's is characterised by loss of neurons and synapses, leading to gradual memory loss and difficulties with language and emotions.

And until now investigations have been limited to 'non-neuronal human cells' or 'animal models'.
However a team from the University of California have developed a way of growing human cells.
Currently there is no cure for Alzheimer’s disease, but medication is available that can slow down its development.

More...
Britons are at their fittest in their 30s (after hitting rock bottom aged 29)
Eating chocolate can stave off bowel cancer, say scientists
The grandma who's a mum again at 53... despite the fact she was still taking the Pill just in case
During the research skin cells from two patients with a rare inherited form of Alzheimer's were taken and used to create neurons displaying biochemical hallmarks of the disease.
Lead researcher Professor Lawrence Goldstein, said: 'Creating highly purified and functional human Alzheimer's neurons in a dish - this has never been done before.
'It's a first step. These aren't perfect models. They're proof of concept. But now we know how to make them.
'It requires extraordinary care and diligence, really rigorous quality controls to induce consistent behaviour, but we can do it.'
Professsor Goldstein highlighted in the paper, published in the journal Nature, that differences between a healthy neuron and an Alzheimer's neuron are subtle.
But being able to grow Alzheimer's neurons will help scientists to better understand how the nervous system is impacted and which drugs would be most effective.
He added: 'We need to do everything we can because the cost of this disease is just too heavy and horrible to contemplate.
'Without solutions, it will bankrupt us - emotionally and financially.'
Further research is now underway.
He said: 'We're dealing with the human brain. You can't just do a biopsy on living patients.
'Instead, researchers have had to work around, mimicking some aspects of the disease in . Neither approach is really satisfactory.'
Alzheimer's disease is the most common form of dementia, which is a group of symptoms associated with a decline in mental abilities, such as memory and reasoning and is most common in people aged over 65.
It attacks nerves, brain cells and neurotransmitters (chemicals that carry messages to and from the brain).
Dementia affects around 5.4 million people in the US, with Alzheimer’s disease responsible for around 60 per cent of all cases.

More promising news on the Alzheimer's research front

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 twitterVancover Sun

BY EVA FERGUSON, POSTMEDIA NEWS

CALGARY — A new study by researchers at the University of Calgary's Hotchkiss Brain Institute is challenging the conventional thinking about how brain cells die in Alzheimer's disease, and may one day lead to effective treatment for the memory-ravaging condition.

Researchers Peter Stys and Gerald Zamponi have shown that brain cells of Alzheimer's patients are dying because of malfunctions in key receptors known as NMDA receptors, which are critical for memory and learning.

"We've shown that the NMDA receptor functions improperly when there is too much alpha beta (a protein) around the ,NMDA receptor" says Zamponi, head of the university's department of physiology and pharmacology.

"So the key now is to find out how to reverse this, and find the right drug that regulates the NMDA receptor."

And by reversing that malfunction, scientists may one day be able to reverse the effects of Alzheimer's.

Zamponi says the University of Calgary is now working with the Centre for Drug Discovery Research and Development in Vancouver, screening hundreds of thousands of drugs to find one that is safe and successfully regulates NMDA.

It may take about two to three years to get to clinical trials, then another four to five years to complete them.

Gaudette says in all his years of working with Alzheimer's patients and their families, this is the most exciting discovery yet, calling it a potential "game changer" for everyone involved in dementia research and care.

"This offers hope. It's a ray of light for people who suffer from this terrible disease."

Alzheimer's disease destroys brain cells and results in memory loss, changes in mood and behaviour, and difficulty with day-to-day tasks.

While it is most commonly diagnosed in adults over the age of 65, more and more cases are being diagnosed in people in their 50s and sometimes even in their 40s.

"Ten years ago, that was unheard of. But we have better diagnoses, better awareness, and people feel more comfortable now getting a diagnosis."

Gaudette encourages anyone who may suspect they are showing symptoms of early onset to go to see their doctor because early diagnoses can lead to early intervention and drug therapy which can significantly slow down progression on the disease.

Zamponi and Stys' research was funded by Alberta Innovates-Health Solutions.

New strategies for treatment of disease of protein unfolding

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

RxPG News


By Northwestern University, [RxPG] Two related studies from Northwestern University offer new strategies for tackling the challenges of preventing and treating diseases of protein folding, such as Alzheimer's, Parkinson's and Huntington's diseases, amyotrophic lateral sclerosis (ALS), cancer, cystic fibrosis and type 2 diabetes.

To do its job properly within the cell, a protein first must fold itself into the proper shape. If it doesn't, trouble can result. More than 300 diseases have at their root proteins that misfold, aggregate and eventually cause cellular dysfunction and death.

The new Northwestern research identifies new genes and pathways that prevent protein misfolding and toxic aggregation, keeping cells healthy, and also identifies small molecules with therapeutic potential that restore health to damaged cells, providing new targets for drug development.

The genetic screening study is published by the journal PLoS Genetics. The small molecule study is published by the journal Nature Chemical Biology.

"These discoveries are exciting because we have identified genes that keep us healthy and small molecules that keep us healthy," said Richard I. Morimoto, who led the research. "Future research should explain how these two important areas interact."

Morimoto is the Bill and Gayle Cook Professor of Biology in the department of molecular biosciences and the Rice Institute for Biomedical Research in Northwestern's Weinberg College of Arts and Sciences. He also is a scientific director of the Chicago Biomedical Consortium.

The genetic study reported in PLoS Genetics was conducted in the transparent roundworm C. elegans, which shares much of the same biology with humans. The small animal is a valued research tool because of this and also because its genome, or complete genetic sequence, is known.

In the work, Morimoto and his team tested all of the approximately 19,000 genes in C. elegans. They reduced expression of each gene one at a time and looked to see if the gene suppressed protein aggregation in the cell. Did the gene increase aggregation or lessen it or have no effect at all?

The researchers found 150 genes that did have an effect. They then conducted a series of tests and zeroed in on nine genes that made all proteins in the cell healthier. (These genes had a positive effect on a number of different proteins associated with different diseases.)

These nine genes define a core homeostastis network that protects the animal's proteome (the entire set of proteins expressed by the organism) from protein damage. "These are the most important genes," Morimoto said. "Figuring out how nine genes -- as opposed to 150 -- work is a manageable task."

In the Nature Chemical Biology study, Morimoto and his colleagues screened nearly one million small molecules in human tissue culture cells to identify those that restore the cell's ability to protect itself from protein damage.

They identified seven classes of compounds (based on chemical structure) that all enhance the cell's ability to make more protective molecular chaperones, which restore proper protein folding. The researchers call these compounds proteostasis regulators. They found that the compounds restored the health of the cell and resulted in reduction of protein aggregation and protection against misfolding. Consequently, health was restored when diseased animals were treated with the small molecules.

Morimoto and his team then conducted detailed molecular analyses of 30 promising small molecules, representing all seven classes. They discovered some compounds were much more effective than others.

"We don't yet know the detailed mechanisms of these small molecules, but we have identified some good drug targets for further development," Morimoto said.

Bingo! Boost thinking skills and keep your mind healthy

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)

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

EmpowHER

In the late stages of Alzheimer’s, patients often spend about half of their time at night awake and a significant part of their daylight hours sleeping.

In extreme cases, people may have a complete reversal of the typical nighttime sleep pattern.

Non-drug treatments seek to create a regular sleep routine, improve the sleeping environment and reduce daytime napping. Non-drug sleep strategies include eliminating alcohol, caffeine and/or nicotine, increasing morning sunlight exposure and encouraging regular exercise (more than four hours before bedtime).

In addition, regular mealtime, bedtime and waking time schedule creates a pattern for the body to emulate. Moreover, it’s suggested that the bed be used only for sleep. Therefore, if the person awakens, discourage him/her from staying in the bed while awake.

In addition, for some reason, television is associated with sleep irregularities for Alzheimer’s patients. Therefore, consider discouraging the person with Alzheimer’s from watching television while awake.

Sources:

Treatments for Sleep Changes. Web. www.alz.org. Accessed 09 Jan. 2012.

Treatments for Alzheimer’s Disease. Web. www. Alz.org. Accessed 09 Jan. 2012.

For Edge on Alzheimer’s, Testing Early Treatments. Web. www.nytimes.com. Accessed 09 Jan. 2012.

Alzheimer’s Disease: Managing Behavior Symptoms without Medication

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


EmpowHER


People with Alzheimer’s may benefit from some of the non-drug approaches to managing behavior symptoms in an effort to promote physical and emotional comfort. Many of these strategies aim to identify and address needs that the person has difficulty expressing as the disease progresses.


Identifying the cause of the problem and/or how the symptoms affect the Alzheimer patient’s experience is also very important. For example, monitor the patient’s comfort by maintaining a comfortable room temperature, checking for pain, constipation, fatigue, any skin irritations, hunger, thirst and/or any infections.


It’s also important to determine whether the person with Alzheimer's disease is just in a bad mood or whether the person is having further symptoms of the disease.


Avoid being confrontational or arguing about unimportant facts. For example, if a person expresses a desire to go to a specific store, don’t point out that the store went out of business five years ago. Rather, you might want to say “That was a great store. I’d love to go there, too.”


Listen to the person’s requests and respond to them. Also, try redirecting the patient by responding to the emotion rather than the behavior. In addition, it may be necessary to change the environment to resolve challenges and obstacles to comfort, security and peace of mind.


Try to maintain a calm environment free from loud noises and/or too much background distraction (e.g., television). And, allow the patient to rest between tiring and/or stimulating events.


Many people with Alzheimer’s experience changes in their sleep patterns. While scientists do not completely understand why this happens, sleep changes somehow result from the impact that Alzheimer’s disease has on the brain.


There is evidence that sleep changes are more common in later stages of the disease, but some studies have also found them in early stages. People with Alzheimer’s disease may feel very drowsy during the day and not be able to sleep at night.


They often become restless or agitated in the late afternoon or early evening.

USF researcher disputes Alzheimer’s as a disease

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

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

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

aol.com

Researchers have found the use of nicotine patches could prevent the deterioration of brain cells and slow down the progress of Alzheimer's disease.

Scientists, whose results were published in the 'Neurology' journal, said the results of a trial on 74 patients with mild cognitive impairment suggested the patches could "slow mental decline".

Nicotine patches slowly release the chemical into the bloodstream and are used by smokers who are trying to quit, in order to get the familiar "hit" of nicotine.

However the scientists found the nicotine played a key role in activating nerve cells which are important for memory and learning.

The people involved in the study, which was carried out at the Vanderbilt School of Medicine, showed an increased attention span and mental function.

Dr Paul Newhouse, who led the study, said: "People with mild memory loss should not start smoking or using nicotine patches by themselves, because of the harmful effects of smoking and a medication such as nicotine should only be used with a doctor's supervision."

'But this study provides strong justification for further research into the use of nicotine for people with early signs of memory loss."

"We do not know whether benefits persist over long periods of time and provide meaningful improvement."

Dr Simon Ridley, of Alzheimer's Research UK, said: "This looks promising. We hope it can help in developing therapies."

Why do old people lose their memory

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

The stereotype of the old forgetful person whose memory often fails him is widely held, but the reason for its appearance was never really pinpointed. Much like gray hair and wrinkles, it was just thought to be part of growing old.

Now new research from Adam M. Brickman, PhD, of the Taub Institute for Research on Alzheimer's Disease and the Aging Brain at Columbia University Medical Center in New York, shows that silent strokes may be the cause. Essentially small dead spots in the brain are found in one out of four elderly people.

Brickman's study is published in the January 3rd issue of Neurology®, the medical journal of the American Academy of Neurology and he states :


"The new aspect of this study of memory loss in the elderly is that it examines silent strokes and hippocampal shrinkage simultaneously."


His study was conducted with over 650 people aged 65 and older. They were free from dementia and were given MRI brain scans. They also took tests to measure their memory, language, speed at processing information and visual perception. Of the 658 people, 174 were identified as having had silent strokes.

Those 174 scored worse on memory tests, regardless of how large their hippocampus was. (The hippocampus is where the brain stores its memories.)

Brickman says that :


"Given that conditions like Alzheimer's disease are defined mainly by memory problems, our results may lead to further insight into what causes symptoms and the development of new interventions for prevention. Since silent strokes and the volume of the hippocampus appeared to be associated with memory loss separately in our study, our results also support stroke prevention as a means for staving off memory problems."


It's not known exactly why or how Alzheimer's destroys the brain's memory, but research has started to show accumulations of proteins called called amyloid plaques, among brain cells. Larger tangled protein strands then start to appear inside the cells. However, treatments to remove the proteins have not been particularly successful in improving memory loss.

Brickman's research points the investigation in a new direction, and focuses more on the vascular system. While circulation and loss of brain function from minute strokes may not be the whole solution its certainly an important part of it, as Brickman concludes :


"What our study suggests is, even when we account for the decline in memory attributed to hippocampal shrinkage or degeneration, that strokes ... play an additional role in the memory decline," Brickman says. He is the Herbert Irving assistant professor of neuropsychology at Columbia University College of Physicians and Surgeons.


Written by Rupert Shepherd
Copyright: Medical News Today
Not to be reproduced without permission of Medical News

Antioxidant found potentially valuable to fight Alzheimer's disease

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
Harold Mandel

Alzheimer's disease is a greatly feared disease. The U.S. National Library of Medicine defines dementia as a loss of brain function which occurs with certain diseases, with Alzheimer's disease (AD), being one form of dementia that gradually gets worse over time. Alzheimer's disease affects memory, thinking, and behavior. Elderly people in Syracuse and their families should be pleased to learn that an antioxidant compound called MitoQ may have the potential to effectively fight Alzheimer's.

The University of Georgia (UGA) News Service has reported "Antioxidant has potential in the Alzheimer’s fight, UGA researchers find." When too much oxidative stress occurs in the brain Alzheimer’s sets in. This is believed to be due to the improper processing of a protein which is associated with the creation of free radicals that cause oxidative stress. A study by researchers in the University of Georgia College of Pharmacy has shown that an antioxidant can delay the onset of all the indicators of Alzheimer’s, including cognitive decline.

An antioxidant compound called MitoQ was administered to mice which were genetically engineered to develop Alzheimer’s. The results of this study have been published in the Journal of Neuroscience. The Alzheimer’s Society says more than 5 million Americans currently suffer from this neurodegenerative disease. It is projected that without successful prevention, almost 14 million Americans will have Alzheimer’s by 2050. This would account for healthcare costs of more than $1 trillion a year.

It is believed that oxidative stress causes neurons in the brain to die which results in Alzheimer’s. Study author James Franklin, an associate professor of pharmaceutical and biomedical sciences, along with Meagan McManus, who received her Ph.D. in neuroscience from UGA, have said “The brain consumes 20 percent of the oxygen in the body even though it only makes up 5 percent of the volume, so it’s particularly susceptible to oxidative stress.”

It was hypothesized by these researchers that antioxidants administered unsuccessfully by other researchers to treat Alzheimer’s were not being concentrated enough in the mitochondria of cells. Mitochondria are structures within cells which have many functions which includes producing oxidative molecules that damage the brain and cause cell death. McManus has said “MitoQ selectively accumulates in the mitochondria. It is more effective for the treatment to go straight to the mitochondria, rather than being present in the cell in general." This study presents an important consideration of the potential for MitoQ to treat Alzheimer's in people.

Antibodies may neutralize Alzheimer's

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

UPI

TROY, N.Y., Dec. 15 (UPI) -- A simple process may make antibodies that neutralize the harmful protein particles that lead to Alzheimer's disease, U.S. researchers suggest.

Antibodies are large proteins produced by the immune system to combat infection and disease. They are comprised of a large Y-shaped protein topped with small peptide loops that bind to harmful invaders in the body, such as a viruses or bacteria.

Once an antibody is bound to its target, the immune system sends cells to destroy the invader, and finding the right antibody can determine the difference between death and recovery, Peter Tessier, assistant professor at Rensselaer Polytechnic Institute in Troy, N.Y., said.

Only a very specific combination of antibody loops will bind to and neutralize each target, and with billions of different possible loop arrangements and sequences it seems impossible to predict which antibody loops will bind to a specific target molecule, Tessier said.

In his research, he uses the same molecular interactions that cause the Alzheimer's proteins to stick together and form the toxic particles that are a hallmark of the disease.

"We are actually exploiting the same protein interactions that cause the disease in the brain to mediate binding of antibodies to toxic Alzheimer's protein particles," Tessier said.

The Alzheimer's antibodies developed by Tessier and his colleagues only latched on to the harmful clumped proteins and not the harmless monomers or single peptides that are not associated with disease.

In the long term, the findings might help develop new drugs to combat Alzheimer's disease, Tessier said.

The findings were published in the journal Proceedings of the National Academy of Sciences.

A New Way to Detect Alzheimer's Disease

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

Cordis Wire



APOE is the main genetic risk factor for this disease, but that is not the whole story; Xabier Elcoroaristizabal is looking for complementary genetic factors
One of our genes is apolipoprotein E (APOE), which often appears with a variation which nobody would want to have: APOEε4, the main genetic risk factor for sporadic Alzheimer’s disease (the most common form in which this disorder manifests itself and which is caused by a combination of hereditary and environmental factors). It is estimated that at least 40% of the sporadic patients affected by this disease are carriers of APOEε4, but this also means that much more still remains to be studied. The researcher at the University of the Basque Country (UPV/EHU) Xabier Elcoroaristizabal has opened up a channel for making a start by analysing candidate genes which, always in combination with APOEε4, could help to explain more cases. His thesis is entitled “Molecular markers in mild amnestic cognitive impairment and Alzheimer’s disease” (Marcadores moleculares en deterioro cognitivo leve tipo amnésico y enfermedad de Alzheimer). An initial article on this can be read in the journal BMC Neuroscience.

The long-term aim is to contribute towards the early detection of Alzheimer’s disease by identifying signs that could be detectable in the very early phases. And, as Elcoroaristizabal explains, while there is no cure for this disorder, the alternative is to get ahead of it and delay its development: “Certain preventive measures involving cognitive stimulation delay its appearance. There are even new drugs that could start to be used earlier. Today there is no solution, but the more we maintain a person’s correct cognitive state, the better.”

Mild amnestic, cognitive impairment

The individuals who develop Alzheimer’s go through a transition period first of all, and this could be the key moment for the effective application of preventive measures. This is mild cognitive impairment (MCI), in which slight cognitive alterations take place but do not affect everyday activities. Among the different types of MCI, one affects memory almost exclusively (amnestic MCI), and those people who suffer from it have a high probability of developing the disorder. The difficult and interesting part is knowing which genetic components are linked to this impairment and also in determining by what percentage the risk of developing the disease increases, a task which Elcoroaristizabal has set himself. “If we can identify which genes are involved and what susceptibility factors there are, preventive measures could be taken,” he explains.

So a contrast study has been carried out among a sample of patients with MCI, ones with Alzheimer’s and healthy people. This can be used to observe the changes and narrow down the field for the zones to be studied, so that candidate genes can be sought there. Elcoroaristizabal himself notes one example among the many others identified: “It has been observed that the brain's capacity to control cholesterol levels seems to play a key role throughout the illness. So, protein encoding genes linked to this control have been analysed.”

In this quest for candidate genes, Elcoroaristizabal has confirmed that the APOEε4 genetic variation is, in fact, the main risk factor for developing Alzheimer’s disease. But it does not end there; he has identified several genes which, as long as they are manifested in combination with APOEε4, could take us one step further towards the early detection of this disorder. “Genes that in some way are connected with neurotransmission channels, oxidative stress or the effectiveness of oestrogens seem to be linked to a greater risk for APOEε4 carriers,” he explains. Specifically, the candidate genes are as follows: COMT (neurotransmission), SOD2 (oxidative stress elimination) and ESR1 and ESR2 (oestrogen action facilitators).

New drug may stop the progression of Alzheimer's disease

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

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

Northern Star

BYRON Bay comedian Mandy Nolan started doing stand-up gigs for people suffering dementia to entertain, but instead she accidentally created a new form of therapy.

Four years after she started working with dementia sufferers, Ms Nolan has developed a program of improvised performance, role playing and theatre sports that has been so successful veteran journalist George Negus is helping put together a documentary on it. "It is really surprising because it was something I was making up as I went along," Ms Nolan said.

"I certainly never intended to create a therapy."

Yesterday, Ms Nolan, Mr Negus and film teachers Russell Burton and Anne Chesher, from the Byron Bay School of Audio Engineering, arrived at Baptist Community Services' Maranoa aged care centre at Alstonville to film the comedian and her patients at work.

Mr Negus said he was keen to help promote the results of the program.

"When somebody said to me this could possibly help get out this message of a hugely beneficial thing for people with Alzheimer's and dementia, I said 'Why not?'," he said.

"If my involvement as a public face helps attract people's attention to this wonderful program then I'm happy to be involved."

Mr Negus said he'd been impressed by what he had seen at Alstonville.

"If you can turn something as serious as Alzheimer's and dementia into a laughing matter, which is what they've done, you're onto something," he said.

"They've turned it not into a joke, but into something you can probably feel better about it if you laugh about it. I've seen it with my own eyes."

The documentary was started by Mr Burton and Ms Chesher after they heard about Ms Nolan's results with dementia sufferers.

The work done yesterday was part of a pilot being put together in the hope of getting approval for a full version, which would air some time next year.

Meanwhile, Ms Nolan will take her Stand Up for Dementia program on the road across Australia to teach 20 new facilitators how to work with those with dementia, thanks to a $47,000 federal grant.

The grant would let Ms Nolan and her husband, Associate Professor John Stevens of Southern Cross University, develop the program further.

"That'll spread the love and the laughter," Ms Nolan said.