Resources

AD Pearls

What are AD Pearls? The brief video below will provide you the answer. This series of courses are now available on the CME/CEU Course Page.

Aricept 23

Amongst the controversy regarding the effectiveness of drugs meant to treat individuals with Alzheimer's, Pfizer recently announced that the FDA has approved a new once daily 23 mg tablet of Aricept, for the treatment of moderate to severe Alzheimer's disease. The approval of this new dose is based on data from a large study of 1,467 participants who received either a 10 mg dose or a 23 mg dose of the drug. In comparing global function via the Clinician's Interview-Based Impression of Change Plus Caregiver Input Scale (CIBIC plus) and cognition via the Severe Impairment Battery (SIB), it was found that while the scores on global functioning were not statistically different between the two doses, that improvements in cognition were statistically higher for individuals receiving the 23 mg dose. It is worth noting that both the CIBIC plus and the SIB have been validated in those with Alzheimer's and other dementias. It is therefore hoped that this higher dose may provide additional symptomatic relief for some patients. The availability of this dose is expected to reach pharmacies in the next couple of weeks.

The press release regarding this new dose can be accessed here.

The growing controversy over the cause of Alzheimer's

The Journal of Alzheimer's Disease has awarded Dr. Rudy Castellani of the University of Maryland with the 2010 outstanding contribution award for his article he wrote in 2009, which critisizes the favored hypothesis, that amyloid plaques are the culprit in Alzheimer's. Instead, Castellani and his fellow researchers believe that focusing on the amyloid proteins is keeping scientists from exploring other potential causes. They believe it is for this same reason, that current treatments remain relatively unaffected. The key points from their article include:

Abnormal accumulations of -amyloid and tau are not necessarily harmful and may simply be the result of earlier problems.
-amyloid may actually be protective, acting as part of a normal immune response, and potentially serving as an antioxident in the brain as well.
There is a poor correlation, at best, between β-amyloid accumulation at autopsy and dementia.
The focus on -amyloid proteins has limited the funding needed to research other hypotheses.

While this team of researchers were not directly involved in the recently proposed change in guidelines for diagnosing and understanding Alzheimer's, the two seem to go hand-in-hand. In short, Castellani may have helped to get the ball rolling in the right direction.

A new day, a new gene

The biology department of MIT is currently researching a gene in the mouse brain, known as SIRT1. This gene has been shown to govern a class of proteins known as situin one, which are involved in cellular regulation of things such as longevity and a cells ability to respond to stress. So far the results indicate that mice with a model of Alzheimer's disease that were genetically engineered to produce more sirtuin one, maintained cognitive abilities as they aged, has less inflammation and fewer plaques in their brain. Mice without this extra sirtuin one, and those who were engineered not to produce any sirtuin at all, showed the steep declines in learning ability and memory as they aged, that is often associated with Alzheimer's. The later group, the SIRT1 knockout mice, showed the greatest declines.
Interestingly, resveratrol may somehow help to increase the expression level of SIRT1, as does caloric- restriction, a diet which has been shown to increase the longevity in just about every living thing. It is for this reason that SIRT1 is often referred to as a longevity gene.

Although previous petri-dish studies have suggested a link between SIRT1 and Alzheimer's, the study at MIT more definitively indicates such a link. SIRT1's specific involvement in the disease comes from the genes ability to cleave amyloid precursor proteins into smaller, harmless, protein fragments.

While these findings certainly provide a degree of hope, the biggest obstacle in creating a drug that increases SIRT1 in humans, will be in finding something that can effectively cross the blood-brain- barrier.

Sharing of Data Leads to Progress on Alzheimer’s

New York Times Article
By GINA KOLATA

Published: August 13, 2010

In 2003, a group of scientists and executives from the National Institutes of Health, the Food and Drug Administration, the drug and medical-imaging industries, universities and nonprofit groups joined in a project that experts say had no precedent: a collaborative effort to find the biological markers that show the progression of Alzheimer’s disease in the human brain.

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