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The Vanishing Mind: Money Woes Can Be Early Clue to Alzheimer's

New York Times Article
By GINA KOLATA

Published: October 31, 2010

An early sign of dementia is an inability to understand money, leaving financial advisers in a bind with clients.

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The Alzheimers Project

Video: Panel discussion on Alzheimer questions

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.

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Where are we with biomarker diagnosis and other tests for Alzheimer's Disease?