President's Message                               1st Quarter 2010

Sleep and Cognitive Function

Dear Friend,

As Americans, our life expectancy has sky rocketed from around age 40 in 1900, to an average age of 76 today. That's over 30 years longer in only 100 years. And a baby born today has the very real possibility of living to 100, and perhaps even longer.

But for millions of people, the price of this increased longevity has come with a horrible loss: their mind and memory. Yes, that's correct. With added life, comes the very real possibility of the development of Alzheimer's disease. Now I recently read a posting on a blog that said: "50% of Americans are doomed to get Alzheimer's." That is simply not true. The statistics on the development of Alzheimer's are scary enough; they don't have to be embellished. The reality is that, unfortunately, if someone lives to age 85, as many more people are now doing, then they have a 50% chance of developing this horrible disease. But that's not everybody.

The greatest concern of people is that they are losing their minds. They usually see small lapses of memory as a sign of major decline. What I would like to discuss in this issue is the importance of being aware of your lifestyle because, as we've been discussing, it's the small things we do every day that count. For example, are you aware that your sleep is a crucial factor in your memory function?

One study that is funded by the National Institute on Aging is examining how poor sleep quality is linked to poor learning in older adults. Scientists believe that it's a combination of sleep elements that contribute to the cognitive decline that we experience as we grow old. Some of these elements are interrupted sleep, processing and storing emotional memories, and motor learning, which is boosted during a particular sleep stage.

Another study in individuals with Alzheimer's disease shows that those suffering from co-occurring depression showed that sleep disturbances to be even more common. Psychosocial interventions, such as sleep restriction, sleep compression, multicomponent cognitive-behavioral therapy and stimulus control were quite effective. Other promising interventions included muscle relaxation and sleep hygiene education.

As we learn more about lifestyle impact on our health and the development of memory loss and Alzheimer's disease, we will continue to share this vital information with you to support you in making positive lifestyle choices.

Sincerely yours,

Dharma Singh Khalsa, M.D.
President/Medical Director

Member Profile

Dr. Perry joined the University of Texas San Antonio faculty in 2006 from Case Western Reserve University  here he was Professor of Pathology and Neurosciences and Chair of the Department of Pathology. He is also distinguished as one of the top 20 Alzheimer's disease researchers with over 800 publications, one of the top 100 most-cited scientists in www.in-cites.com/nobel/2007-neutop100.html Neuroscience & Behavior and one of the top 25 scientists in Free Radical research. He currently serves as and President for the American Association of Neuropathologists. He is on the editorial board of over 60 journals including American Journal of Pathology and Journal of Biological Chemistry, and is Editor-in-Chief of Journal of Alzheimer's Disease.

Research Interests

Our studies are focused on the mechanism of formation and physiological consequences of the cytopathology of Alzheimer disease. We have shown that oxidative damage is the initial cytopathology in Alzheimer disease. We are working to determine the sequence of events leading to neuronal oxidative damage and the source of the increased oxygen radicals. Our current studies focus on (i) the mechanism for RNA-based redox metal binding; (ii) the consequences of RNA oxidation on protein synthesis rate and fidelity; (iii) the role of redox active metals in mediating prooxidant and antioxidant properties; (iv) the signal transduction pathways altered in Alzheimer disease that allow neurons to evade apoptosis; and (v) mechanism of phosphorylation control of oxidative damage to neurofilament proteins.

News

FDA Approves Generic Aricept to Treat Dementia Related to Alzheimer's Disease

According to a recent press release by the FDA, the U.S. Food and Drug Administration approved the first generic versions of Aricept (donepezil hydrochloride) orally disintegrating tablets on Dec. 11, 2009 Donepezil hydrochloride is indicated for the treatment of dementia related to Alzheimer's disease.

Orally disintegrating tablets dissolve on the tongue, without having to be swallowed whole. This may make it easier to take the medication for older or disabled patients who have difficulty swallowing.  

"Generics offer greater access to health care for all Americans," said Gary Buehler, director of the FDA's Office of Generic Drugs. "Health care professionals and consumers can be assured that FDA-approved generic drugs have met the same rigorous standards as the brand-name drug  and are the same as the branded in dosage form, safety, strength, route of administration, quality, performance characteristics and intended use." 

Alzheimer's disease is an irreversible, progressive brain disease that slowly destroys memory and thinking skills and, eventually, the ability to carry out the simplest tasks of daily living. In most people with Alzheimer's disease, symptoms first appear after age 60. Alzheimer's disease is the most common cause of dementia among older people, but it is not a normal part of aging.

Dementia refers to a decline in cognitive function that interferes with daily life and activities. Alzheimer's disease starts in a region of the brain that affects recent memory, then gradually spreads to other parts of the brain.

The generic donepezil hydrochloride orally disintegrating tablets, manufactured by Mutual Pharmaceutical of Philadelphia, have been approved in 5 milligram and 10 mg strengths.

For more information:
Consumer Education: Generic Drugs
http://www.fda.gov/Drugs/ResourcesForYou/ucm167906.htm

News

Infections 'speed memory loss'

Infections outside the brain may speed memory decline in Alzheimer's disease, UK researchers say.

  In a study of 222 elderly people with Alzheimer's they found that getting infections in places like the chest or urinary tract could double memory loss.

  The Southampton University researchers think this leads to higher levels of an inflammatory protein called tumour necrosis factor (TNF) in the blood.

  They say better care to prevent infections is very important.

Cognitive decline

  The study published in the journal Neurology followed the Alzheimer's patients for six months.

  Between them 110 of the 222 subjects developed a total of 150 infections, in areas such as the chest, stomach and intestines and the urinary tract, which led to the production of TNF proteins.

  These are collectively known as acute systemic inflammation events (SIEs).

"The worse the infection the worse the effect on the memory"
Professor Clive Holmes, University of Southampton

  Subjects with one or more SIEs during the six months follow-up had two times the rate of cognitive decline from their baseline score at the start of the study compared with those who had no SIE.

  And those patients who had high baseline levels of TNF and then suffered an SIE over the following six months had a 10 fold increase in the rate of cognitive decline compared to those who were SIE free.

Further work

  Professor Clive Holmes at the University of Southampton, who led the research, said they had looked at patients with mild, moderate and severe Alzheimer's disease.

  "The worse the infection the worse the effect on the memory, but this is only an association at the moment.

  "One might guess that people with a more rapid rate of cognitive decline are more susceptible to infections or injury, but we found no evidence to suggest that people with more severe dementia were more likely to have infections or injuries at the beginning of the study.

  "It's important that older people, people with dementia and carers treat any infection seriously and seek medical help"
Dr Susanne Sorensen, Alzheimer's Society

  "If further work proves that TNF is causing more brain inflammation it may be possible to use drugs that block TNF to help dementia sufferers."

  Professor Holmes said although common illnesses like colds and slight wounds could also set up an inflammatory response in the body, the data from his study did not support the idea that even these could cause memory loss.

Inflammatory processes

  Dr Susanne Sorensen, Head of Research, Alzheimer's Society said: "This study is an important step towards understanding the processes that occur during the onset of Alzheimer's disease.

  "We know there might be a link between inflammatory processes and Alzheimer's but this is not yet fully understood.

  "These findings are helping us to understand more about possible reasons for this link.

  "In the meantime it's important that older people, people with dementia and carers treat any infection seriously and seek medical help. "

  Rebecca Wood, Chief Executive of the Alzheimer's Research Trust said: "This fascinating study shows that infections and inflammation may be linked to memory loss in Alzheimer's.

  "We need to do more research into this and all aspects of the disease to understand its causes."