APP -- Good, bad or both?

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EurekAlert

by Karen Mallet

CHICAGO – New data about amyloid precursor protein, or APP, a protein implicated in development of Alzheimer's disease, suggests it also may have a positive role -- directly affecting learning and memory during brain development. So is APP good or bad? Researchers at Georgetown University Medical Center say both, and that a balance of APP is critical.

Alzheimer's disease, the fourth leading cause of death in the United States, is characterized by neuronal cell death and a progressive loss of functioning in the brain. Symptoms of Alzheimer's (AD) include memory loss and impaired judgment. Abeta is one of many proteins found to be associated with the disease. It is released when APP, a larger protein, is cut by several enzymes. Research suggests this occurs when APP is abnormally processed, possibly due to trauma, cholesterol levels or oxidative stress. When Abeta is released, it can form plaque, a contributing factor in AD. Thus, Abeta and APP are involved in the early process of AD development.

APP is also known to be present at the synapses between neurons though its molecular action is not understood. Synapse loss is thought to be one of the main contributors to the cognitive decline seen in AD.

In a presentation at the 39th annual meeting of the Society for Neuroscience, Georgetown University Medical Center researchers say that while APP is negatively associated with AD, it appears to play a critical role in brain development.

Many studies have elucidated the importance of synapses and dendritic spines, the protrusions that allow communication between brain neurons, in learning and memory. In this new research, the GUMC scientists found decreased spine density in mice that have been genetically modified to not produce APP. The scientists then looked at four-week-old mice that over produced APP and found a significant increase in spine density. At one year old, however, these mice have Abeta plaques, as well as a decrease in spine density due to the effect of Abeta, which is known to be neurotoxic.

"Our work suggests that APP balance is critical for normal neuronal development, connection of synapses, and dendritic spine development, all of which have implications for the extensive synapse loss and cognitive decline seen in Alzheimer's disease," explains the study's author, Hyang-Sook Hoe, PhD, a research scientist in the department of neuroscience. "One strategy to counteract development of Alzheimer's disease is to maintain balance in APP protein expression in order to prevent production of Abeta."

Half of Patients With Alzheimer's Disease Adhere to Cholinesterase Inhibitors After 1 Year: Presented at ANA

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DG Dispatch

By Charlene Laino

BALTIMORE, Md -- About half of patients with Alzheimer's disease who have been prescribed oral cholinesterase inhibitors are still taking the medication after 1 year, researchers said here at the American Neurological Association (ANA) 134th Annual Meeting.

"Optimal compliance and persistence rates of oral cholinesterase inhibitors -- rivastigmine, galantamine, and donepezil -- are important factors contributing to the beneficial impact of these therapies," said Francis Vekeman, MA, BSc, Groupe d'analyse, Ltee, Montreal, Quebec, Canada, in his October 13 poster presentation.

Vekeman, a specialist in health economics and health policy, said, "Based on real-world data from a large cohort of Alzheimer's disease patients initiated on cholinesterase inhibitors, 50% were compliant during the first year following cholinesterase treatment initiation."

But persistence in taking the medication was lower, he said. After 1 year, just 36% of patients completed criteria for persistence in taking their medication. The researchers defined persistence as continuous drug use without a gap of 30 days or more between medication refills at any time after treatment initiation.

"Only 20% of the patients were persistent with their oral cholinesterase inhibitors at 2 years after initiating therapy," he said.

The researchers accessed the MedSatat MarketScan database and reviewed data on 17,717 patients who were prescribed rivastigmine, donepezil, or galantamine between January 2004 and June 2008v

During the study period, the researchers found that 15,008 patients began therapy using donepezil, 1,480 patients initiated therapy on galantamine, and 1,240 patients initiated therapy with rivastigmine. Vekeman also noted that 3,370 of the patients were being treating with antipsychotics at the time they initiated cholinesterase inhibitor therapy.

After 12 months, Vekeman determined that compliance for all patients was 49.9%. If the patients were taking memantine in addition to their cholinesterase inhibitor therapy, the compliance rate was higher, at 59.3%. But if patients were just taking 1 of the 3 oral cholinesterase inhibitors, the compliance rate was 45.9%.

Vekeman said the study, based on pharmacy claims, includes some inherent limitations, including that a filled pharmacy prescription does not guarantee that patients actually took the medication. He said that these studies also cannot assure that the billing diagnoses and pharmacy dispensing data are accurate. He added that the study did not give researchers the ability to determine the severity of illness among the patients.

The research was supported by Novartis Pharmaceuticals Corporation, East Hanover, New Jersey

Dementia may lead to hallucinations

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SouthBendTribune.com

Debbie Haws

The progression of dementia on memory and cognition may lead to personality and behavioral changes that include hallucinations, delusions and paranoia. Let’s begin by defining the terms.

Hallucination is a false perception that appears to be real. For example, a man dying of thirst in a desert thinks that he sees an oasis. It is so real to him he drinks the sand. Hallucinations are sensory experiences. They can appear in the form of visions, voices or sounds, feelings, smells or tastes. I hear something, I smell something, I feel something on my skin that is not there. A dream isn’t a hallucination because you aren’t awake or conscious. Hallucinations can be induced by drugs, including LSD and certain strong types of marijuana. Hearing the voice of, or briefly seeing, a loved one who has recently died can be a part of the grieving process.

Delusion is a fixed persistent belief. I believe this thing to be true no matter what you say. I believe you are my mother and no matter how many times you tell me different I'm going to insist you are my mother. The most common are delusions of persecution, jealousy and grandeur (I'm a rock star or on a “special mission”).

Paranoia is an extreme, irrational distrust of others. For instance, a person with dementia might believe that the nursing home is trying to poison their meals or perhaps that staff members or family are stealing from them. They may feel that someone is following them or “out to get them.”

It is very common with this disease process for people to misperceive occurrences in their environment. Sometimes this may happen because the individual is over stimulated and there is too much noise and chaos or they are under stimulated and they are feeling isolated. If the TV is on in the background with other conversations and noises, they make think the voices from the TV are real. If they are under stimulated and don’t have structured activities, they have a tendency to disconnect or pull back, creating isolation for themselves. This allows the opportunity for more delusions and hallucinations.

People lose memory in the reverse way they acquire it. The things learned very early as a child and in young adult life are the things that stay well into the end of the disease process. The most recent information _ adult children, a second marriage, career _ is the first lost. Their reference to people are usually relationships from long ago. Through their eyes they are young, so it doesn't make sense to them that they would have an adult child; therefore, "you must be my sister because I'm too young to have a daughter." You may look very similar to someone they remember from their past so that’s who you become.

At other times, they may think their reflection in the mirror is a stranger and become frightened; or think it must be their mother who came to visit.

Hallucinations and delusions can be ignored if they are harmless and do not cause the person to become agitated. Allowing them their own idea of truths and understanding is an actual nurturing process. Supporting their reality is very important.

To help them move past a hallucination, it may help to focus their attention on an activity or concentrate on their favorite hobbies. If they feel someone is watching them, close the curtains or blinds on the windows or cover the mirror. Keep their area well lit and reduce background noises.

When paranoia and delusions becoming life threatening, such as refusing to eat for an extended time for fear of it being poisoned, it may require professional intervention. This condition can be related to psychosis, an underlying condition that happens sometimes as the disease progresses. Psychosis is an actual break in reality and may call for anti-psychotic medication and temporary clinical treatment. That's not true for everyone.

Behavior that is caused by this disease process happens progressively and over a long time. If the onset of symptoms occurs quickly, from one day to the next, it is probably not disease oriented, but a result of health and medical problems, such as infections, fatigue or nutrition. Arrange for a medical checkup to eliminate the presence of physical or psychiatric problems and to check the effects of medication.

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Dementia Linked to High Cholesterol

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EmpowHer

According to the National Institutes of Health, dementia rarely begins before age 60, and the risk of developing dementia increases with age. Degenerative dementia, which is caused by Alzheimer's disease and vascular dementia, cannot be reversed. Other forms of dementia caused by brain tumors, metabolic causes, infections, low vitamin B12 levels, normal pressure hydrocephalus and thyroid conditions, on the other hand, can be treated.

The Mayo Clinic describes dementia as “a group of symptoms affecting intellectual and social abilities severely enough to interfere with daily functioning,” rather than a specific disorder. Symptoms of dementia include changes in feeling or perception, altered sleep patterns, decreases in problem-solving skills and judgment, disorientation, learning problems, impaired recognition, language problems, short-term and long-term memory problems, motor system problems, hallucinations and delusions, confusion and....... read more of Dementia Linked to High Cholesterol

Does Smoking Marijuana Help Prevent Dementia? Part 2

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EmpowHer

Results

Despite the dearth of publications on the topic of marijuana, only one small study met the above criteria but the data were presented in such a poor fashion that the scientists could not extract any meaningful data for analysis.

The single study data was not only insufficient but the results showed no effects of marijuana on individuals with dementia. Analysis of the data found that marijuana did not improve behavior, symptoms of dementia nor did it improve mental performance or cognition. The conclusion was that more randomized double-blind placebo controlled trials are needed to determine whether marijuana is clinically effective in the treatment of dementia.

Conclusion

To date, there is......read more of Does Smoking Marijuana Help Prevent Dementia

Does Smoking Marijuana Help Prevent Dementia? Part 1

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EmpowHer

Over the past few years, scientists have discovered the presence of a cannabinoid organization and the recognition of specific cannabinoid receptors in our brains. A lot of work has been done to determine why this system is present in our brain, how it works, and what it does. No one knows for sure what is the exact role of cannabinoids in our brain, but some experts believe that they may play a role in regulating production of other neurotransmitters and help prevent or worsen brain injury or delay deterioration of neurons. Deterioration of neurons is a common feature in several types of dementia, including Alzheimer’s disease, and for this reason, many scientists are wondering if cannabinoids may be clinically useful in the treatment of the individuals. Recent experimental evidence does reveal that cannabinoids may help in interrupting processes that lead to development of Alzheimer’s dementia.

To determine whether cannabinoids or marijuana is clinically useful in the treatment of dementia, Cochrane registry reviewed several health data studies. The data looked at all randomized controlled trials, which have assessed the efficacy of marijuana at different doses in people with dementia.,,,read more of Does Smoking Marijuana Help Prevent Dementia

Web can help elderly surfers slow dementia

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TimesOnLine

Jonathan Leake, Science Editor


GOOGLING is good for grandparents. Internet use can boost the brain activity of the elderly, potentially slowing or even reversing the age-related declines that can end in dementia, researchers have found.

Using brain scans, they found the internet stimulated the mind more strongly than reading, and the effects continued long after an internet session had ended.

“We found that for older people with minimal experience, performing internet searches for even a relatively short period of time can change brain activity patterns and enhance function,” said Gary Small, professor of neuroscience and human behaviour at University of California, Los Angeles (UCLA).

In the research, Small and his colleagues worked with 24 men and women aged between 55 and 78. Half of them had used the internet a lot; the others had little experience.

At the start of the research, they were asked to conduct a series of internet searches while their brains were scanned using a technique known as functional magnetic resonance imaging (fMRI). This measures changes in blood flow around the brain to work out which parts are the most and least active.

After the initial scan, participants went home and used the internet to carry out specified tasks for an hour a day at least seven times over the following fortnight. Then they had a second brain scan, again while searching the internet.

Small and his colleagues found the impacts began immediately, with the first scan demonstrating brain activity in regions controlling language, reading, memory and vision.

By the time of the second scan, however, the activated areas had spread to include the frontal gyrus and inferior frontal gyrus, areas known to be important in working memory and decision-making. The researchers suggest internet searching stimulates brain cells and pathways, making them more active.

“Searching online may be a simple form of brain exercise that might be employed to enhance cognition in older adults,” said Teena Moody, a UCLA researcher who co-

wrote the report with Small. Moody believes internet searching challenges the brain more than reading because people need to perform several tasks at once. These include holding important information in their own memory while simultaneously assessing the information on screen and extracting the parts they want from graphics and words.

The research will be presented tomorrow at the annual meeting of the Society for

Neuroscience in Chicago, where the impacts of ageing on the brain are a big theme.

It has long been known that as people age, their brain functions and abilities also change. In many respects these changes are beneficial — verbal and social skills tend to improve until at least late middle age, for example. In other areas there can be declines. One of the best known is mathematics, as shown by the number of mathematicians and physicists who do their best work early and then struggle to match their youthful performances.

It is only in recent years, however, that researchers have been able to use technologies such as fMRI to observe the brain in action and measure the changes that come with age. What they have found is that as people age, their brains undergo structural and functional changes, often including atrophy, reductions in cell activity and increases in deposits of insoluble protein. All of these can reduce cognitive function.

In Britain, for example, around 700,000 people suffer from dementia, a condition in which so much of the brain has died that function is severely impaired.

Small and Moody’s argument is that brains are similar to muscles, in that the more they are exercised, the healthier they become. So, activities such as internet use, reading and socialising can slow or reverse normal age-related declines.

Small said: “Our most striking finding was that internet searching appears to engage a greater extent of neural circuitry that is not activated during reading.”

Other neuroscientists support the idea of exercising the brain but question the benefit of spending too much time on the internet

The genetic component of Alzheimer’s disease identified

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Destination Sante

A Franco-European research team has identified two factors associated with genetic predisposition to Alzheimer’s disease.
Their research is still in the early stages but this discovery could eventually offer hope to millions of sufferers across the world. The genomes of more than 20,000 people were analysed, among them 6,000 individuals suffering from Alzheimer’s disease.

Through this research they were able to isolate two new genes that appear to be closely associated with the disease. Their role in the appearance of the disease is not yet known, the report’s authors warn. So caution is needed. And it must be said that numerous routes have already been explored in the fight against Alzheimer’s disease, but without great success. The reason being, that like so many chronic conditions, the disease seems to be linked to complex interactions between genetic and other environmental-type factors.
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Source : INSERM,

Genetic testing for disease heredity gains favor

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detnews.com

Kim Kozlowski / The Detroit News
The sequencing of the human genome has revolutionized scientists' ability to better understand hereditary diseases and created more opportunities for people to get tested.

But as genetic information further increases understanding of health, researchers are starting to ask: Do people want to know if they are predisposed to a disease, even if there is no cure?

Two recent studies indicate the answer is yes -- even though the medical establishment is apprehensive about predictive testing on children for incurable diseases.

Contrary to concerns that genetic testing for Alzheimer's disease might cause angst among people who discover they are predisposed, most did not suffer any major distress, a University of Michigan study showed in July.

Meanwhile, more than one-third of parents say they would be interested in knowing if their children might develop a disease for which there is no cure, according to a study published last month in the online edition of the journal Pediatrics.

"The ability to know things is coming," said Beth Tarini, assistant professor of pediatrics at the University of Michigan Medical School and author of the study on genetic testing of children.

"The question from the medical community is, 'How do we deal with this because we no longer are going to be the gatekeepers?' "

There are several kinds of genetic testing, said Emily Edelman, project director of the National Coalition for Health Professional Education in Genetics.

Genetic tests are used to predict diseases and to diagnose symptoms.

But a growing number of companies are offering direct-to-consumer genetic tests for analysis of predisposition to a number of diseases, such as Type 2 diabetes, restless leg syndrome, Parkinson's and other diseases.

Though some companies involve doctors, many bypass the medical establishment, giving consumers the power to seek out personal genetic information by ordering kits online and sending saliva directly to testing labs.

The Genetic Information Nondiscrimination Act, which went into effect this year, bans discrimination of individuals by insurance companies or employers based on information detected by genetic tests.

With companies giving people a choice and federal law offering protection, people are interested in getting genetic information because it helps them make life decisions.

"I realize with this knowledge I really need to live my life fully in the moment," said Solange Muller, who found out in 2005 that she has a 52 percent chance of developing Alzheimer's by the time she reaches 85.

Muller always knew she was at risk because her mother developed the incurable disease when she was 65. Though the test results shook her at first, she used the information to start doing things more often that she enjoys, like traveling and visiting museums.

"I really changed the quality of my life," she said.

New Report Shows Number of Medicines In Development in New York to Treat Diseases Affecting Women

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Reuters

COLD SPRING HARBOR, N.Y -- America's
pharmaceutical research and biotechnology companies are working on nearly
1,000 life-changing medicines for diseases affecting women, according to a new
report released by the Pharmaceutical Research and Manufacturers of America
(PhRMA). The medicines are awaiting approval by the U.S. Food and Drug
Administration or are in human clinical trials.


In the U.S., diseases that disproportionately affect women include diabetes,
which has reached epidemic proportions and affects 11 million women
nationwide. Autoimmune diseases strike women three times more and anxiety and
depression two times more women than men. The number one killer of American
women is heart disease.


Breast cancer is the most frequently diagnosed cancer in American women. To
help raise awareness about this disease, Medicines in Development Women 2009
is being released during Breast Cancer Awareness Month.


According to the New York State Department of Health, breast cancer is the
second-leading cause of cancer-related death among women in New York State.
Last year, about 14,000 women in New York State were newly diagnosed with
breast cancer, and more than 2,900 women died from the disease. New York women
also have a higher incidence rate of cervical cancer than that of the national
average, according to the Centers for Disease Control and Prevention.


The report lists 969 new medicines in development. They include 112 new
treatments for breast cancer, 86 new treatments for obstetric/gynecologic
conditions, 76 for asthma, 114 for autoimmune diseases, 155 for diabetes, 131
for arthritis, and 80 for Alzheimer's disease.


One medicine in the report is a potential cutting-edge treatment that attacks
the cause of Alzheimer's disease rather than merely treating its symptoms.
Currently, treatment options for Alzheimer's disease are limited. This
groundbreaking medicine holds the potential to slow the progression of the
disease and could vastly improve quality of life of Alzheimer's patients.
Women account for 70 percent of Alzheimer's deaths.


"America's pharmaceutical research and biotechnology companies continue making
exciting progress in the search for new cures and treatments for diseases of
special concern to women," said PhRMA Senior Vice President Ken Johnson, in
his remarks at the press briefing at the Cold Spring Harbor Laboratory on Long
Island, New York. "We live in an era of medical discovery in which we
understand more and more about the unique biological and behavioral
differences between men and women and their respective health care needs. This
knowledge is inspiring a continuing medical revolution that is bringing new
hope to women around the world in the form of promising new treatments and
cures."


During the press briefing, Academy Award- and Tony-winning actress Marcia Gay
Harden and American pop icon Deborah Gibson described the personal experiences
that led them to advocate for women's health issues.


Harden was inspired to become an advocate while preparing for the role of a
woman with breast cancer in the film Rails and Ties. "My character had Stage
Four breast cancer and a mastectomy, so as part of researching my role we
brought a group of breast cancer survivors to the set," explained Harden.
"Meeting these women was transformative for me and helped me realize what a
problem breast cancer is. I welcome the chance to raise awareness about it."


Gibson, who had a No. 1 hit song at 16 years of age, explained that it was the
stressful experience of being a child celebrity that led to her battle with
anxiety and depression. "You see a lot of professional children who grow up to
have problems, because fame is not a natural thing we're wired to know as kids
how to handle," said Gibson. "Once I was able to acknowledge what it [anxiety
and depression] was, I was able to get help through therapy and medication."


"We are pleased to participate in events that promote the development of new
drugs that will save women's lives," said Geri Barish, president of 1 in 9:
Long Island Breast Cancer Action Coalition. "With over 40,000 women still
dying of breast cancer every year, it is these new drugs that hold the promise
to help eradicate breast cancer or at least relegate it to a chronic
condition. These new drugs promise us something we breast cancer survivors
need--hope."


New York Biotechnology Association executive director Nathan Tinker noted that
incredible progress is being made by America's biotechnology and
pharmaceutical research companies in developing new and more effective
treatments for the wide range of diseases that affect women. "Cooperation
between the country's educational facilities, research hospitals,
laboratories, and innovative biopharmaceutical companies has proven critical
to this success," said Tinker.


"While scientists are making exciting progress in the search for new cures and
treatments, these efforts are wasted if the medicines we develop aren't
accessible to patients who need them," said PhRMA's Johnson.


Help is available to patients in need through the Partnership for Prescription
Assistance (PPA), a program sponsored by America's pharmaceutical research
companies. To date, the PPA has helped nearly six million patients nationwide,
including more than 193,000 people in New York. Since its launch in April
2005, the PPA bus tour has visited all 50 states and more than 3,000 cities to
educate people about patient assistance programs.


The "Help is Here Express" is staffed by trained specialists able to quickly
help uninsured and financially struggling patients access information on more
than 475 patient assistance programs, including nearly 200 programs offered by
pharmaceutical companies. When the "Help is Here Express" moves on, patients
can visit PPA's easy-to-use Web site (www.pparx.org) or call the toll-free
phone number (1-888-4PPA-NOW).


The Pharmaceutical Research and Manufacturers of America (PhRMA) represents
the country's leading pharmaceutical research and biotechnology companies,
which are devoted to inventing medicines that allow patients to live longer,
healthier and more productive lives. PhRMA companies are leading the way in
the search for new cures. PhRMA members alone invested an estimated $50.3
billion in 2008 in discovering and developing new medicines. Industry-wide
research and investment reached a record $65.2 billion in 2008.

Turmeric Alzheimer's Cure

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Scientists learn more about the health benefits of various spices and herbs every day. Turmeric shows promise in helping people stave off Alzheimer's disease. Alzheimer's disease robs people of their minds because of the build up of amyloid plaques and neurofibratory tangles in their brain. Studies show that consuming tumeric prevents this from happening in mice. People who live in India rarely develop Alzheimer's disease, but eat foods containing curry powder, which always contains turmeric. Consuming turmeric is safe, but always consult your doctor before taking any new spice or herb.

Alzheimer's disease
Alzheimer's disease, the most common form of dementia, progresses over time. Symptoms include problems with thinking, memory and behavior. More than 5.3 million Americans exhibit symptoms of Alzheimer's disease. The frequency of getting this disease increases as you age. Every year the government and individuals in the United States spend more than $100 billion treating Alzheimer's disease.

Beta Amyloid Plaques
Beta-amyloid plaque appear in the brain of a person with Alzheimer's disease. They consist of abnormal protein accumulation that, over time, results in inflammation of nerves which stops nerve signals from getting from one part of the brain to another part. Eventually the brain cells die, leaving the Alzheimer's sufferer with memory loss, thinking difficulties and behavior issues.

Curcumin
Turmeric comes from curcumin. You find it in curries and other spicy dishes from India, Asia and the Middle East. Like many other herbs, people first used curcumin as a seasoning. Later, people used it for medicinal purposes. Indian medicine has used turmeric to relieve pain and inflammation in the skin and in muscles for centuries.
In India, very few people get Alzheimer's Disease. Researchers TP Ng, PC Chiam, T Lee, HC Chua, L Lim, EH Kua published an article in the American Journal of Epidemiology in 2006 entitled "Curry consumption and cognitive function in the elderly." In this study, they investigated the association between the curry consumption and cognitive level in 1,010 Asians between 60 and 93 years of age. The study found that those who ate curry once a month or more scored better on cognitive tests than those who ate curry rarely or never.

Benefits of Curcumin
Because of curcumin's anti-inflammatory properties, it may have a role in curing Alzheimer's Disease. Curcumin acts as an antioxidant, too. It inhibits the formation of free radicals. It decreases bad cholesterol. Small amounts of curcumin given over longer periods of time is better than taking a large dose all at once.
Safety of Curcumin
No one reported serious side effects of taking tumeric thus far, but long-term use in high doses causes liver toxicity. For this reason, avoid......read all of Turmeric Alzheimer's Cure

Olive oil compound linked to Alzheimer's

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UPI.com

CHICAGO, Oct. 17 (UPI) -- A compound in olive oil targets and blocks toxic proteins that damage brain cells and cause memory loss in Alzheimer's disease victims, U.S. researchers said.

The compound, oleocanthal, alters the structures of the proteins, ADDLs, said William L. Klein of Northwestern University and Paul A.S. Breslin of Monell Chemical Senses Center.

"Binding of ADDLs is thought to be a crucial first step in the initiation of Alzheimer's disease," Klein said in a statement. "Oleocanthal alters ADDL structure in a way that deters the protein from binding to synapses that allow the nervous system to connect."

ADDLs bind within the synapses of the brains of Alzheimer's patients and are believed directly to disrupt nerve cell function, eventually leading to memory loss, cell death and global disruption of brain function, the researchers said.

Klein and colleagues identified ADDLs in 1998, leading to a major shift in thinking about the causes, progression and treatment of Alzheimer's disease. ADDLs are structurally different from the amyloid plaques that accumulate in brains of Alzheimer's patients.

Future studies are needed to......read more of Olive oil compound linked to Alzheimer's

How to Apply a Person Centred Approach to Dementia Care

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eHow

A symposium in April 2008 helped change the thinking about nursing homes. The theme of the discussion, called "Creating Home in the Nursing Home," was person-centered care and living surroundings.

With this theme in mind, accomplish person-centered care in a nursing home by creating a homelike atmosphere.and centering residents' care on their interests, talents and preferences. Understand the individuality of each resident with dementia. An atmosphere that works for one person may not work for someone else. Preferences and needs may change from day to day. Awareness of the whole person challenges the caregiver. Bringing a smile to the faces of people who have dementia rewards those who care for them.

Step 1Get a family history of the resident's past interests, jobs, siblings, children and hobbies by talking to family members, friends and the resident.

Step 2Communicate with the resident in a way that he can best understand, using verbal reminders, gestures, written messages, or whatever it takes. He may have trouble finding words. Fill in the blanks for him. At the same time, compliment him.

Step 3Observe the resident in his new environment. See what time he gets up naturally. Detect his current likes and dislikes. Determine what his behaviors are and what sets off problem behaviors.

Step 4Nip agitated behavior in the bud. Divert and redirect. Do something to stop the unwanted behavior, then redirect him to another activity.

Step 5Set his new room up with favorite items from his former home. Provide him with necessities like a television, clock, easy reading material or other things that delight him and improve his quality of life.

Step 6Discover tips for environmental modifications that make life easier for the resident and the caregiver.

Step 7Keep the resident safe. New surroundings and diminished identification skills might combine to put him at risk of interacting with his environment in a dangerous way; for example, he might try to eat inedible objects.

Step 8Make sure you address the resident's cultural needs.

Step 9Allow the resident to engage in group activities and in individual activities designed specifically for him. Adapt and modify an activity he used to enjoy.

Step 10.......read all of Apply a Person Centred Approach to Dementia Care

Sleep Problems & Alzheimer's Type Dementia

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eHow

Inability to get a good night sleep and resulting daytime drowsiness is displayed in many older adults, especially those with Alzheimer's disease or other forms of dementia. Sleep problems contribute to physical deterioration and mood problems. Caregivers of those with Alzheimer's disease have difficulty getting a good night's rest because of the patient's wandering, getting out of bed repeatedly and talking in bed.

A program of stimulating daytime activity for those with Alzheimer's disease and education for their caregivers may be helpful in controlling sleep problems. Prescribing sleep medicines is an option, too.

Alzheimer's Disease
Alzheimer's disease, a brain disorder, is the most common form of dementia. Dementia, a general term for memory loss, difficulty learning and behavior changes, seriously interferes with daily life including problems sleeping. Many people with Alzheimer's disease exhibit changes in their patterns of sleep. Scientists do not completely understand why this occurs.

Normal Aging Sleep Changes
As we age our sleep changes. Sleep quality, quantity and type of sleep change. Older people have more trouble falling asleep and sleep for a shorter period of time. The time you are in deep sleep decreases, as well, as you age.
Sleep changes in Alzheimer's disease
Many people with Alzheimer's disease wake up more often and stay awake longer during the night. Brain wave studies display decreases in both dreaming and non-dreaming stages of sleep. Those who cannot sleep may wander, be unable to lie still or call out, which disrupts the sleep of their caregivers.
Daytime napping is common because of Alzheimer's medications. Because of napping during the day, night time sleep diminishes. Persons with Alzheimer's disease often become restless or agitated in the late afternoon or early evening. This is called "sundowning." As Alzheimer's disease progresses, these individuals spend more time in bed sleeping during the day and less time sleeping at night

Treatment Without Medication
There are some simple lifestyle changes that can help a person with Alzheimer's sleep better at night, according to a study called Nighttime Insomnia Treatment and Education for Alzheimer's Disease: A Randomized, Controlled Trial, published in the Journal of the American Geriatrics Society in May, 2005. Learning about good sleep habits, the benefits of moderate exercise and spending time in the sun helped those with Alzheimer's disease, this study reports.
Caregivers should........read all about Sleep Problems and Alzheimer's Type Dementia

Skills tests like 'connect the dots' may be early Alzheimer's indicator

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Washington University News

By Michael Purdy

A study of mental decline in the years prior to diagnosis of Alzheimer's disease suggests that changing the focus of testing may allow physicians to detect signs of the disease three years earlier.

Current cognitive testing typically focuses on episodic memory, or the ability to remember things like word lists or information from a reading. But scientists at Washington University School of Medicine in St. Louis found that another class of mental abilities known as visuospatial skills begins to deteriorate up to three years prior to diagnosis. These skills are tested with tasks such as connecting the dots or using a guide to build a structure with blocks.

"We may need to rethink what we look for as the earliest signs of mental change associated with Alzheimer's disease," says senior author James Galvin, M.D., a Washington University neurologist who is also on staff at Barnes-Jewish Hospital. "If we can better recognize the first signs of disease, we can start treating patients earlier and hopefully with new treatments we can slow or perhaps even stop their progress into dementia."

The results are published in the October issue of Archives of Neurology.

Galvin and his coauthors analyzed long-term data from volunteers at the Memory and Aging Project at Washington University's Alzheimer's Disease Research Center (ADRC). For three decades, researchers have been regularly conducting extensive testing of volunteers to uncover the factors associated with the normal, healthy retention of mental function in seniors. The new study analyzes data on 444 volunteers aged 60 to 101 that were gathered between 1979 and 2006.

Scientists categorized cognitive testing results into a global measure of cognitive abilities as well as three specific types of mental skills: episodic memory, visuospatial skills and working memory, which assesses the ability to manipulate facts from memory, such as repeating a list of numbers backwards.

Declines in episodic memory and working memory became discernible a year before volunteers were diagnosed with Alzheimer's disease. Losses in the composite assessment of cognitive abilities were detectable two years prior to diagnosis, and visuospatial skills began to decay three years earlier. According to Galvin, the losses in visuospatial skills were particularly noticeable if testing tasks were timed.

Researchers also analyzed the data using a new model that not only tracks the speed of decline in a mental ability but also the acceleration of the decline. Episodic memory's decline accelerated more slowly than that of both visuospatial skills and working memory, which declined fastest.

The new perspective may allow doctors to detect signs of Alzheimer's earlier, but more information will be needed to make a firm diagnosis. To make that possible, researchers at the ADRC are trying to take what they've learned in the new study and correlate it with biomarkers, which are physical changes associated with preclinical Alzheimer's disease. These include such tests as scanning the brain for amyloid plaques or analyzing the levels of proteins in the cerebrospinal fluid.

Amyloid brain plaques, a primary characteristic of Alzheimer's disease, can begin building in patients 10 years or more before clinical symptoms become apparent, Galvin notes.

"The new findings raise the question of what changes are occurring in the brain during the one- to three-year period prior to diagnosis," Galvin says. "Patients have had plaques in their brain for years, and suddenly their cognitive abilities begin to deteriorate. Is a threshold being crossed where brain cell death begins to occur or really starts to pick up speed?"

Galvin and his coauthors also plan to apply their new approach for assessing mental decline to other dementias including Lewy body dementia and the form of dementia associated with Parkinson's disease.

The Most Common Cause of Dementia

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eHow

What Is Dementia?
Dementia, an abnormal brain condition, is when your brain cells progressively die, causing memory loss, trouble thinking, learning and perceiving, as well as problems with behavior. The most common cause of dementia is Alzheimer's disease. Scientist have not identified any single reason why the brain cells of people with Alzheimer's disease die, but they know some risk factors that increase your chances of getting Alzheimer's disease. They also know that the accumulation of two abnormal proteins in the brain plays a role in causing Alzheimer's disease.

Controlable Risk Factors
Serious head injuries increase your chances of developing Alzheimer's disease. To protect your head from injury, buckle your seat belt when you are riding in a car, wear a helmet when you participate in sports and keep clutter to a minimum in your home.

Keep your heart and blood vessels healthy too, because your risk of developing Alzheimer's disease increases from having conditions that damage your heart or blood vessels, such as heart disease, stroke, high blood pressure, high cholesterol and diabetes. Work with your doctor if you have any of these conditions.

Findings of research reported in July 2009 at the Alzheimer's Association International Conference on Alzheimer's Disease in Vienna show that living a healthy lifestyle diminishes your chances of getting Alzheimer's disease. This means maintaining a normal weight, avoiding tobacco, staying socially active and exercising your mind and body regularly.

If you suspect you may have Alzheimer's disease, make sure to get checked out by a doctor because some diseases and underlying conditions cause symptoms similar to Alzheimer's disease. These include vitamin B12 deficiency, malnutrition, hypothyroidism and hypoglycemia.

Uncontrollable Risk Factors
As you age, your chances for developing Alzheimer's disease increases. After age 65, the likelihood of you getting Alzheimer's disease doubles. According to Dr. Samuel Gandy, an Alzheimer's research director, having a family member with Alzheimer's disease doubles your risk of developing Alzheimer's disease. Plus, abnormal proteins appear in the brains of those with a genetic risk at a much higher rate than normal.
Plaques and Tangles
As you get older.......read all of Most Common Cause of Dementia

Naturopathic Vascular Dementia Treatment

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eHow

Vascular dementia is a term describing difficulty in thinking, memory and behavior caused by the narrowing of blood vessels in the brain. Curing vascular dementia is unlikely no matter what treatment you use. Natuopathic or conventional treatments can slow down the progression of the dementia

Naturopathic Treatment
Naturopathic treatmentNaturopathic treatment uses the body's natural healing abilities to remedy or cure diseases. Included as part of natural medicine are mental and physical exercise, eating healthy, stress reduction and taking natural solutions. Naturopathic treatment complements traditional medicine. It treats the whole person.

Increase Antioxidant Consumption
Antioxidants in fruits and vegetablesResearchers from King's College, London found noteworthy proof that antioxidants called flavonoids, found in red wine, cocoa and many fruits and vegetables, increase blood flow to the brain thereby reducing brain cell death and improving brain function in many people with vascular dementia. The body produces antioxidants to defend itself against free radicals in our body, including our brain. Free radicals destroy or render cells useless by attacking the cell membranes, Common thinking is that the brain attacks free radicals there with the formation of plaques and tangles if we do not consume enough antioxidants to do the job. Get antioxidants from eating a healthy diet rich in fruits and vegetables, and supplement with vitamins A, E, C, B-complex and D. Follow the recommended dosage prescribed by your doctor.

Music Therapy
Music stimulates the brainNew research from the University of California-Davis uncovers associations between music and memory, according to the article "New Music Therapy Research" in the March 1, 2009 issue of Dementia Today. Music elicits strong responses from people with vascular dementia, calming agitated behavior often seen in people with the disease. Listening to music acts as a trigger to old memories. Even those who do not speak can sing many of the words to familiar songs. Exposing people with dementia to music at least once a day helps them retrieve memories that might otherwise be forgotten. Any activity stimulating the brain is a good natural treatment for those with vascular dementia.

Other Mind-Stimulating Activities
Sharing a photographMany activities stimulate the brain of persons with dementia. It depends what the person liked predementia. Involvement in activities slows down the progression of the dementia, elevates the mood of people with dementia, decreases agitated behavior and gives them a feeling of self-worth. Besides music and musicals, doing word puzzles, reading easy short books, looking at pictures--especially baby pictures--and playing simple card games all keep their brain active and are natural with no side effects.

Physical Exercise
Exercise is goodA new study in the Journal of the American Medical Association finds that exercise can slow down memory loss even in those who are already having difficulty, such as those with vascular dementia. Physical exercise costs nothing and is good for both the body and the brain. Like mental exercise, physical exercise slows the decline associated with vascular dementia, elevates the mood of people with dementia, decreases agitated behavior and reduces stress. Walking, simple aerobic exercise including water aerobics, movement to music and sitting exercises all benefit persons with vascular dementia and treats the dementia naturally. Check with a doctor before starting any exercise program.

Homocysteine Reduction
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New Findings About Brain Proteins Suggest Possible Way To Fight Alzheimer's (part 2)

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ScienceDaily

Dr. Herz said the study is especially important because this mechanism involves another protein involved in Alzheimer's called ApoE4, which is the primary risk factor for the most frequent late-onset form of the disease. The receptor that binds to ApeE molecules also binds to Reelin, and is part of the red-light/green-light complex that controls the sensitivity of the NMDA receptors.

"These results imply that Reelin, ApoE and beta-amyloid converge on the same molecular mechanism, which is critical in the Alzheimer's disease process, and Reelin may be a common factor to fight both beta-amyloid and mutated ApoE," Dr. Herz said. "This study establishes a rationale that ApoE receptors have an action that can keep the Alzheimer's disease process at bay by preventing damage in the first place."

The researchers are currently studying the role of ApoE4 in this mechanism. Mimicking or preserving normal Reelin function to stimulate the ApoE receptors might provide a path to stave off the disease, Dr. Herz said.

Other UT Southwestern authors included lead author Dr. Murat Durakoglugil, assistant instructor of molecular genetics; graduate student Ying Chen; Dr. Charles White, professor of pathology; and Dr. Ege Kavalali, associate professor of neuroscience.

The study was funded by the National Institutes of Health, the American Health Assistance Foundation, the Perot Family Foundation and the Humboldt Foundation.

New Findings About Brain Proteins Suggest Possible Way To Fight Alzheimer's (part 1)

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ScienceDaily — The action of a small protein that is a major villain in Alzheimer's disease can be counterbalanced with another brain protein, researchers at UT Southwestern Medical Center have found in an animal study.

The findings, available online in the journal Proceedings of the National Academy of Sciences, suggest a promising new tactic against the devastating illness, the researchers said.

The harmful protein, called beta-amyloid, is found in the brain and, when functioning properly, suppresses nerve activity involved with memory and learning. Its normal function can be likened to a red traffic light, restraining nerve cells from getting overexcited when they receive stimulating signals from neighboring cells. People with Alzheimer's disease, however, accumulate too much beta-amyloid – the traffic light gets stuck on "red" and nerve cells become less responsive.

Another brain protein, called Reelin, acts as a "green light," stimulating nerve cells to respond more strongly to their neighbors' signals.

The new study shows that applying Reelin directly to brain slices from mice prevents excess beta-amyloid from completely silencing nerves.

"If we can identify a mechanism to keep the nerve cells functioning strongly, that might provide a way to fight Alzheimer's disease," said Dr. Joachim Herz, professor of molecular genetics and neuroscience at UT Southwestern and the study's senior author.

In the study, the researchers recorded electrical currents in the mouse hippocampus, an area of the brain associated with learning and memory. From their experiments they determined that Reelin and beta-amyloid interact with the same protein complex, called an NMDA receptor, which plays an important role in coordinating chemical signals between adjacent nerve cells.

They found that Reelin activates and strengthens the response of the NMDA receptor. In the presence of too much beta-amyloid, the receptor migrates into the cell, reducing the cell's sensitivity to incoming signals. By contrast, in strong concentrations of Reelin, the receptor remains active and the cell has the green light to continue receiving normally.

Dr. Herz said the study is..........comeback tomorrow to read part 2 of.... New Findings About Brain Proteins Suggest Possible Way To Fight Alzheimer's

Olive oil and dementia(part 2)

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Dronmore Leader

Where did the story come from?The research was carried out by Dr Jason Pitt and colleagues from the Northwestern University, the University of Pennsylvania, Western Illinois University and Rutgers University in the US and the Universidade Federal do Rio de Janeiro in Brazil.

While the authors provide grant numbers for those that support their research, it is unclear what funding organisations provided these.

The study was published in the peer-reviewed medical journal Toxicology and Applied Pharmacology.



What kind of scientific study was this?Alzheimer’s disease is the most common form of dementia, affecting around 420,000 people in the UK. It is a degenerative brain disorder. The exact causes aren’t well understood, but plagues and tangles made of proteins form around brain cells, eventually leading to their damage and death. This causes a range of symptoms that can include confusion, mood swings, poor memory and forgetfulness and more severe symptoms such as delusions or obsessive behaviour.

Research has demonstrated that certain fibres called Aß-derived diffusible ligands (ADDLs) in the brain are the main chemicals responsible for the initiation of Alzheimer’s disease. In this laboratory study, researchers explored the neuroprotective properties of a chemical called oleocanthal, which is derived from olive oil.

The researchers prepared ADDLs in the laboratory and investigated the effects of various concentrations of oleocanthal on these molecules. They assessed the effect of this extract on the primary molecules (monomers) that make up the ADDLs and also on the formed ADDLs (which are chains of monomers).

They also explored the effects of oleocanthal on nerve cells from the hippocampus, an area in the brain that plays an important role in memory and learning. The hippocampus is one of the areas in the brain affected by Alzheimer’s disease. Previous research has established that ADDLs of a certain size can bind at the synapses (junctions between neurones in the brain) The loss of synaptic function that results is a crucial first step in the development of Alzheimer’s disease.



What were the results of the study?The study found that in the presence of the chemical oleocanthal, the ADDLs became more immunoreactive (i.e. more likely to provoke an immune response) and less soluble (which may lead to a decrease in toxicity).

When the chemical was applied to the brain cells, ADDLs formed in the presence of oleocanthal were less likely to bind to the synapses and this was accompanied by reduced deterioration of these cells.



What interpretations did the researchers draw from these results?The researchers say their results suggest that oleocanthal is capable of altering the chemicals implicated in Alzheimer’s disease and can also protect against the effects of these compounds on synapses in the brain. They say that this suggests oleocanthal may be a key compound in the development of treatments for Alzheimer’s disease.



What does the NHS Knowledge Service make of this study?Previous research has indicated that phenols (a group of chemical compounds) such as oleocanthal may have neuroprotective properties, and this laboratory study has uncovered some of the complex reactions that may explain these effects.

More research is needed to establish exactly how it protects nerve cells, (for example, whether it actually reduces binding at the synapses or whether the protective effect is due to the changes in the structure of ADDLs that it causes).

The researchers report that, overall, their findings are consistent with other studies that have investigated phenolic compounds such as oleocanthal and demonstrated protective effects. This extract from olive oil and other similar molecules may have a role to play in future development of drugs for Alzheimer’s disease, but these will require further research and development. The drug development process is a long one, which starts with studies such as these in the laboratory and later move through animal testing to safety and efficacy studies in humans.

While the chemical being tested here - oleocanthal – is an extract from olive oil it has not been tested in humans with Alzheimer’s yet. Also, whether these particular effects will be derived from eating olive oil itself is not clear from these findings. Olive oil is likely to be part of a traditional Mediterranean diet, which is also high in vegetables, fruits and fish, and while there is some evidence that a Mediterranean diet reduces the risk of Alzheimer’s disease it is not clear what specific role olive oil has to play in these benefits. Only further studies can answer these questions.

Olive oil and Alzheimer's disease(part 1)

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Dronmore Leader

Olive oil could hold key to defeating Alzheimer's," reported the Daily Express. The newspaper reported that a compound found in the oil has been shown to slow down changes in the brain that lead to Alzheimer's disease. According to the paper, researchers believe that the antioxidant that gives the oil its 'peppery bite' will become a key ingredient in new drugs.

This laboratory study investigated the effects of an olive oil extract (oleocanthal) on chemicals thought to be involved in Alzheimer’s disease. It found that nerve cells exposed to oleocanthal were better protected from the effects of these potential neurotoxins.

However, this study does not indicate that increasing olive oil consumption will protect from Alzheimer’s disease. The olive oil extract and other similar molecules may have a role to play in future development of drugs for Alzheimer’s disease, but these will require considerable further research and development. It will be some time before the direct relevance of these findings to preventing Alzheimer’s are clear, but this is the first step in the process.

Where did the...... come back tomorrow for part 2 of Olive oil and dementia

Coffee Does Little to Protect the Aging Brain

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ABC News

NEW YORK (Reuters Health) - Sorry coffee lovers -- downing a few cups of coffee throughout the day may spark alertness, but it's unlikely to protect the aging brain from mental decline or dementia, according to researchers from Finland.

Some studies have suggested that coffee has a protective effect on brain function in old age, while others have not shown this association.

One of the latest studies on the topic, which appears in the September issue of the American Journal of Clinical Nutrition, found no association between coffee consumption and declining cognition or dementia scores in either men or women.

Dr. Venla S. Laitala, at the University of Helsinki, and colleagues assessed the coffee drinking habits, as well as other social, demographic, and health data, of a large population of twin pairs who were 50 years old on average.

At this point in time, 75 percent of the men and 83 percent of the women drank more than 3 cups of coffee a day. Only 4 of men and about 1 percent of women reported no daily coffee consumption.

When the group was just over 74 years on average, the investigators conducted telephone interviews in 2,606 of the study participants (48 percent women) to specifically screen for declining cognition and dementia.

They found that each year of increasing age was associated with declines in thinking abilities, regardless of gender.

However, in this study, middle-age coffee consumption was not protective against "cognitive decline or preventive against dementia," Laitala told Reuters Health in an email correspondence.

As expected, heart disease, diabetes and dissatisfaction with life were significantly associated with lower cognitive performance, the researchers report.

Therefore, Laitala's team suggests further investigations concentrate on the role heart disease, diabetes, and life satisfaction play in altered and age-related thinking and analytic abilities.

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Religious Commitment as a Sign of Mild Dementia?

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Christianity Today

Sarah Pulliam Bailey

The New York Times writes about science and faith in a profile of the new National Institutes of Health head Francis Collins, author of The Language of God: 'A Scientist Presents Evidence for Belief

Collins resigned in August from from the BioLogos Foundation, the foundation he started as a way to reconcile faith and science. At the time, he noted concerns people had about his outspoken faith. Here's The Times' take:

First, there is the God issue. Dr. Collins believes in him. Passionately. And he preaches about his belief in churches and a best-selling book. For some presidential appointees, that might not be a problem, but many scientists view such outspoken religious commitment as a sign of mild dementia.

And the Wall Street Journal strikes back:

It seems unlikely that scientists think religious commitment is literally a symptom of dementia. What the Times is really saying is that "many scientists"--how many is not specified--are prejudiced against religious people. It's one of the few prejudices the Times would discuss so glibly.

This is the second time that The New York Times' Gardiner Harris has outlined concerns about Collins's faith. In July, The Times published an op-ed from Sam Harris criticizing Collins's appointment.

Francis Collins is an accomplished scientist and a man who is sincere in his beliefs. And that is precisely what makes me so uncomfortable about his nomination. Must we really entrust the future of biomedical research in the United States to a man who sincerely believes that a scientific understanding of human nature is impossible?

Collins's appointment received both praise and criticism from conservative Christian groups after his appointment.

Autopsies shine light on dementia

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Subjects of decade-long studies continue to aid researchers in death

Star Bulletin

By Helen Altonn

Investigators led by Dr. Lon White of the Pacific Health Research Institute have done about 800 autopsies on the men, recruited in 1965 for a study of heart disease and stroke, at Kuakini Medical Center with family permission.

The Honolulu-Asia Aging Study was expanded over the years with research and significant discoveries on diseases associated with aging. The program has received more than $72 million in federal funds since the 1960s.

Only about 400 of the original 8,006 men are still living. Kuakini is receiving $1.1 million in federal funds to continue the research.

The men in the study group were born from 1900 to 1919 and identified through World War II Selective Service registration files. The youngest now living is 90, White said.

Pacific Health Research Institute doctors and associates have followed the men, assessing their cognitive, motor and sensory functions; lifestyle; health; and illnesses. Now, as they do autopsies, White said, "we are in a unique position to understand the causes and meanings of those changes we see in the brain."

With the volunteers who "signed onto a lifetime study" 44 years ago, White said the team is striving for basic understanding to prevent or slow the progression of dementia and "turn around those we could turn around."

Fewer than six studies worldwide are looking intensely at dementia and Alzheimer's disease. The Honolulu study has been a leader with some findings "revolutionizing the way people think about these diseases," White said.

"We have been able to correct a huge number of important misunderstandings related to the causes of dementia," he said, adding that "loss of cognition late in life is a whole lot more complicated than we used to think it was."

He said the researchers found processes contributing to dementia that have been attributed incorrectly to Alzheimer's disease.

For example, they have found changes in tiny arteries of the brain produced by a vascular disease, molecular changes often seen in Parkinson's disease in the cerebral cortex, which has a role in memory, and loss of neurons in the area of the brain associated with memory.

While the researchers are interested in the causes of death, White said, "We're more interested in the value of what we can learn from these for the rest of the world and future of people."

He said they are.....read all of Autopsies shine light on dementia

Rethinking Alzheimer's disease and its treatment targets

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PhysOrg.com) -- Psychiatry professor George Bartzokis introduces a new theory about the fundamental cause of Alzheimer's and other neurodegenerative diseases.

The standard explanation for what causes Alzheimer's is known as the amyloid hypothesis, which posits that the disease results from of an accumulation of the peptide amyloid beta, the toxic protein fragments that deposit in the brain and become the sticky plaques that have defined Alzheimer's for more than 100 years.

Billions of dollars are spent yearly targeting this toxic peptide — but what if this is the wrong target? What if the disease begins much earlier, fueled by a natural process? Reporting in the current edition of the journal Neurobiology of Aging, UCLA professor of psychiatry George Bartzokis argues just that and says that a better working hypothesis is the "myelin model."

"The greatest promise of the myelin model of the human brain is its application to the development of new therapeutic approaches," Bartzokis said.

Like insulation around wires, myelin is a fatty sheath that coats our nerve axons, allowing for efficient conduction of nerve impulses. It is key to the fast processing speeds that underlie our higher cognitive functions and encoding of memories.

But the lifelong, extensive myelination of the human brain also makes it uniquely vulnerable to damage. The myelin model's central premise is that it is the normal, routine maintenance and repair of myelin throughout life that ultimately initiates the mechanisms that produce degenerative diseases like Alzheimer's. That is, the amyloid-beta peptide and the tau peptide, which is also implicated in Alzheimer's, as well as the signature clinical signs of the disease, such as memory loss and, ultimately, dementia, are all byproducts of the myelin breakdown and repair processes.

"The pervasive myelination of our brain is the single most unique aspect in which the human brain differs from other species," said Bartzokis, who is a member of the Laboratory of Neuro Imaging in the UCLA Department of Neurology and a member of UCLA's Brain Research Institute. Myelin is produced by oligodendrocytes, specialized glial cells that themselves become more vulnerable with age.

Bartzokis notes that myelination of the brain follows an inverted U-shaped trajectory, growing strongly until our 50s, when it very slowly begins to unravel as we age. The myelin that is deposited in adulthood ensheaths increasing numbers of axons with smaller axon diameters and so spreads itself thinner and thinner, Bartzokis said. As a result, it becomes more susceptible to the ravages of age in the form of environmental and genetic insults and slowly begins to break down faster than it can be repaired.

The exclusive targeting of the amyloid-beta peptide for many years is understandable because the same genes and enzymes involved in controlling myelination and myelin repair are, ironically, also involved in the production of amyloid-beta proteins. Bartzokis' point is that the amyloid beta may actually develop as a result of the natural process of the repair and maintenance of myelin.

"So the breakdown that leads to Alzheimer's and other age-related brain diseases, such as Parkinson's, may begin much earlier, before the formation of the protein deposits that are used to define these diseases," Bartzokis said.

Most drugs being developed for Alzheimer's are targeting amyloid beta, but little if any clinical improvement is being seen. This is, according to Bartzokis, "similar to cleaning up a house that's been flooded by water but never repairing the actual pipe that created the flood.

"For drug development then, the targets should be much further upstream, earlier in the process before the AB plaques even develop," he said.

Instead of focusing on reducing amyloid beta, Bartzokis argues, the myelin model suggests entirely different approaches to treatment and prevention of Alzheimer's disease that precede plaque formation. With modern brain imaging technology, clinicians could track the dynamic changes taking place in the brain and intercede well before any signs of Alzheimer's are seen.

"With earlier intervention," Bartzokis said, "we could reduce and potentially eliminate the increasingly catastrophic burden of dementia on the individual and their family, the health care system, and our society."

Alzheimer's chemicals may be natural part of brain function

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Deseret News

By Elizabeth Stuart

natural part of human brain function, recent research suggests.

"You are actively forgetting and remembering all the time," said Dr. Dale Bredesen, founding president and CEO of the Buck Institute for Age Research, during a presentation Tuesday at the University of Utah. "Alzheimer's disease is just a fundamental imbalance in those signals."

Most researchers look at Alzheimer's as a disease of toxicity, said Bredesen, who works out of Novato, Calif.

"It's like having acid on your brain," he said. "Something's eating it."

But the chemical associated with tissue destruction in Alzheimer's patients is also present in the brains of young, healthy people — a phenomenon none of the more than 500,000 scientific papers published on the topic can explain.

"We argue the amyloid beta peptide does have a normal function," Bredesen said. "We think Alzheimer's is more of a signaling disorder rather than a disease of toxicity."

Bredesen's theory links brain development to brain deterioration.

As a fetus grows, it produces more nerve cells than it will ultimately use. Some of those cells build connections with one another, some die. Both outcomes are determined by naturally occurring chemicals.

Alzheimer's disease, said Bredesen, is an out-of-control example of this same process.

"The amyloid beta peptide in your brain is doing what it's supposed to do, but there's a thousand times too much of it," he said.

Bredesen and his colleagues believe netrin-1, another naturally occurring protein, has the opposite effect as amyloid beta peptide.

Preliminary lab tests using mice infected with "Mouzheimer's" support this theory. After just 10 days of treatment, mice injected with netrin-1 showed behavioral improvement.

"The idea is if you insert amyloid beta peptide into the receptor, it'll tell your nerve cell to start packing up and moving out," he said. "When you insert netrin-1, the cell gets the signal to start setting up for a party

Halftime: New NFL stadium, in this economy?

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USA Today

The Minnesota Vikings' strategy is becoming transparent. First they, they woo a legend out or retirement. Then they have him throw a miracle touchdown pass, raising Super Bowl expectations.

Then they hit up taxpayers for $700 million.

That's how much the Vikings say they need for a new stadium, and the campaign begins in earnest today, in meetings with political leaders. The pay-us-or-lose-us threat is implicit in a comment from Vikings VP Lester Bagley, to the St. Paul Pioneer-Press.

Said Bagley: "If the answer is no, then why would you own a team in this market?"

Not exactly a slogan the Chamber of Commerce is going to jump on.

A similar rumbling is emanating from Jacksonville, where Sunday's Jaguars-Titans game may have 20,000 empty seats, just like the home opener. Jaguars owner Wayne Weaver got together with local sports media, to clarify his comment about possibly playing a future game in Orlando.

Weaver downplayed the lure of playing at Orlando's Citrus Bowl, saying, "I don't think they have the kind of facility that would accommodate the kind of revenues you have to derive out of an NFL stadium."

But what I'm reading between the lines there is Weaver telling Orlando that, "Hint, hint, my team will be a free agent in two years, which is plenty of time to get your stadium up to speed. Call me."

And no, the L in NFL has never stood for loyalty.

Here are some more lunchtime topics to munch on:

. . . The New York Times has a followup to its report on NFL players being far more susceptible to dementia than the general population. The Times says the NFL's disability plan isn't structured to consider dementia an occupational risk, which drastically reduces benefits.

The league's response was that it's a union matter that needs to be addressed during collective bargaining. Meantime, the NY Daily News has a story on Jets defender Eric Smith reflecting on the aftermath of his concussion, and how he kept knocking things over every time he went to the refrigerator.

Not an occupational risk?

. . . Big Ben Roethlisberger skipped out on his normal weekly media chat yesterday. That left everyone to wonder whether it's because another casino-related lawsuit against him has surfaced or maybe because the coaches are chafed about him organizing a team road trip to WWE's Monday Night Raw.




. . . Worth the click: Life.com is commemorating the anniversary of Hank Aaron's final game (Oct. 3, 1976) by making him a "guest editor" and posting a very cool photo gallery.
. . . It hasn't taken Herschel Walker long to get in the swing of his new MMA career. He's already challenged UFC president Dana White to a fight. And how long until we get him matched up against Jose Canseco?

. . . I'm an Orioles believer. And I firmly believe they'll get the one additional defeat they need to tie the team's second-worst losing streak all-time of 14 straight.

. . . Can someone please grab me an Ozzie Smith bobblehead at the Cardinals' game tomorrow night?

. . . Mateen Cleaves led Mighigan State to a Final Four title in 2000, and now he's paying homage to coach Tom Izzo, naming his son Mateen Izzy Cleaves. Hope that works out better than that dreaded Izzy mascot of the 1996 Atlanta Olympics.

. . . In addition to getting to the wedding altar at light speed to marry Khloe Kardashian, the Lakers' Lamar Odom also recently took up boxing. Hmmmm. Do you suppose too much time in the ring led to the hasty offering of an engagement ring?

. . . Here's the toddler version of the speech Herb Brooks gave before pulling off the Miracle on Ice.

. . . Big Papi must be having indigestion after seeing the way his restaurant got hammered in a Boston Globe review.

. . . Sad to hear that ever since middle school the Vikings' Percy Harvin has suffered from serious migraines. But, as that 101-yard return against San Francisco proved, he also can give them.

. . . Drew Brees, on why he won't be getting tattoos like those of Saints teammate Jeremy Shockey: "No, I’ll leave that to him. You have to have biceps of a certain size to have tattoos and I’m not in that category."

. . . And the Orlando Magic's Rashard Lewis would love for you to give him a call. Seriously.

Can You Catch Alzheimer's?

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

It's a memory-destroying disease that has baffled scientists for decades, but one researcher has a controversial theory: that we can catch it with a kiss.
By Tom McGrath, Men's Health

Rich P. is only in his 20s, but these days he finds himself obsessing over something most guys his age never think twice about: Am I doomed to lose my mind?

In some ways, Rich's anxiety is understandable. "My girlfriend is a social worker who works with the aged, specifically people with Alzheimer's," he says. "So I've seen close up what the disease does to you." Indeed, Alzheimer's disease is characterized by memory loss and confusion, and typically ends with complete disconnection from the world. People in its advanced stages can't care for themselves, recognize loved ones, or remember the lives they lived. (Worried about losing your memory and health as you age? Discover the age erasers for men that can strip away 10 years and leave you looking and feeling younger, longer!)

There's also another, even more personal connection for Rich: His girlfriend's father recently passed away from Alzheimer's. He was one of more than 70,000 Americans who die from the disease every year.

Still, what should worry Rich most isn't what he's witnessed in other people, but what he sees in the mirror. Because there, literally right under his nose, is evidence that the monster that could be responsible for Alzheimer's is already skulking about inside his body, preparing itself, at some point, decades down the road-to attack and destroy his brain.

So here's the question: Is it in you, too?

For years, physicians and Alzheimer's experts have said that the earliest symptoms of the disease typically don't appear until you're in your 60s, 70s, or beyond. But now there's reason to believe that the first warning signs may actually crop up much earlier than that, and in a seemingly much more benign way: as cold sores, those embarrassing blisters that can erupt on the lips of people who are sick or run-down.

The sores are triggered by the herpes virus—most often, herpes simplex virus type 1 (not to be confused with HSV-2, which predominately causes genital herpes). In recent years, a growing body of research, much of it championed by a British scientist, has begun to suggest a startling fact: The same virus known for sabotaging people's social lives could be responsible for the majority of Alzheimer's cases.

"There's clearly a very strong connection," says the researcher, Ruth Itzhaki, Ph.D., speaking one afternoon in her office at the University of Manchester, in northwestern England. A neurobiologist, Itzhaki has spent the better part of two decades studying the link between herpes and Alzheimer's. "I estimate that about 60 percent of Alzheimer's cases could be caused by the virus."

As viruses go, herpes is a particularly devilish bugger. The ancient Greeks were among the first to record the sores it causes (the virus' name is derived from a Greek word meaning "to creep"), and today the microbe is ubiquitous. As many as 85 percent of us have been infected by it, though experts say as few as 15 percent show symptoms. Worse, once you have it, you have it forever: After the initial infection, the virus lies dormant in your peripheral nervous system, occasionally flaring up during periods of stress, illness, or fatigue. You can follow these three steps to prevent a herpes outbreak, but it never completely disappears.

And it's that fact—herpes as the viral equivalent of The Thing That Wouldn't Leave—that lies at the heart of the herpes-Alzheimer's relationship. Research suggests that as we age, HSV-1 actually spreads to our brains, where in certain people, Itzhaki theorizes, it can cause the buildup of deposits—known as amyloid plaques and neurofibrillary tangles—that attack and destroy the cells responsible for memory, language, and physical functions. In short, those people develop Alzheimer's.

It's a provocative theory, one that would sound preposterous if it weren't for the steadily accumulating evidence. Last January, for instance, Itzhaki and her colleague, Matthew Wozniak, Ph.D., published a study in the Journal of Pathology in which they searched for the presence of the herpes virus in people's brains. They found that it resided in 90 percent of the amyloid plaques

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