Dimebon and the Amyloid Hypothesis

Contributed by: Dennis Fortier, President, Medical Care Corporation

Among the many interesting studies presented this week at the ICAD conference in Vienna, Austria , one that has generated lots of discussion looked at Dimebon's potential impact on the amyloid load in the brain.

As you may recall from an earlier post, many experts believe that an accumulation of beta-amyloid is the primary cause of Alzheimer's disease. This theory is currently driving the majority of drug development work.

Dimebon, an antihistamine, appears to improve cognition through a loosely understood improvement of mitochondrial function. However, through ongoing research to better understand how Dimebon works, scientists have recently looked at its impact on the amyloid load. To most everyone's surprise, mouse brain cells in a dish produced much higher amounts of the amyloid proteins when combined with Dimebon. This finding sits in stark contrast to the expected reduction in amyloid that the prevalent hypothesis suggests.

These results raise new questions about the mechanism of Dimebon and suggest that the amyloid hypothesis, if valid, may well be more complicated than initially believed. In any case, this study contributes new information to the process of understanding Alzheimer's pathology and provides the scientific community with a new set of potentially fruitful questions to explore.

1 comment :

  1. What's really intriguing here is that beta-amyloid increased (in vitro) with Dimebon - but patients who took Dimebon had improved scores in cognition and functional tests. So, beta-amyloid increased - and cognition improved - ?! Conventional beta-amyloid=evil idea may not be that simple. Beta-amyloid may only be a byproduct of other processes - or could be that Dimebon is helping to 'dump' beta-amyloid out of other areas or cells, and into harmless deposits - or ?