Amyloid Hypothesis Evolving?

Contributed by: Dennis Fortier, President, Medical Care Corporation

A hallmark lesion of Alzheimer's disease, to the extent that it is currently understood, is the accumulation of amyloid plaques in the brain. Most experts agree that amyloid plays some central role in the disease pathology but there is little consensus about what that role might be.

New research out of the Mount Sinai School of Medicine and published in the Annals of Neurology suggests strongly that it is the free floating clumps, or oligomers, of amyloid protein that cause the brain damage and cognitive decline, and not necessarily the dense amyloid plaques that form when these oligomers aggregate.

While this finding helps to clarify the role of amyloid in a very complex process, there are still some key weaknesses in the amyloid hypothesis that must be explained. Primarily, we need to understand why some people with excessive plaque formation have no symptoms of Alzheimer's disease. If the free floating oligomers are present prior to plaque formation, then one would presume that symptoms of decline would manifest by the time the plaques are present.

Nonetheless, this scientific advance will most likely drive the ongoing focus of scientific inquiry to an earlier point in the amyloid cycle.

This is a perfect example of how the scientific process uncovers the answers to such complex problems: questions are identified, hypothesis are formed, conclusions are drawn, and the questions are modified. The process repeats and renews until the pieces of the puzzle are clearly exposed and fitted together.

Click this link to review prior discussions on the amyloid hypothesis.

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