Refining the Amyloid Hypothesis

Contributed by: Dennis Fortier, President, Medical Care Corporation

A leading theory about Alzheimer's Disease (AD) suggests that toxic plaques of beta-amyloid protein accumulate in the aging brain, destroy neurons, and cause declining cognitive function. This theory has been deeply scrutinized and modified over the past two decades of intensive research.

The notable, but poorly understood role of amyloid has driven both treatment strategies and diagnostic strategies for Alzheimer's Disease. In fact, a great majority of efforts to treat Alzheimer's disease have been based on agents that either slow production of amyloid, alter the form of amyloid, or remove amyloid from the brain. Likewise, many diagnostic approaches have been driven by measures of the amount of amyloid in the brain or spinal fluid.

New research from the Penn Medicine Department of Radiology, published in the Neurobiology of Aging, suggests that the location of amyloid plaques in the brain may be more important that the amount of amyloid in the brain. In fact, it has been widely observed (but as yet unexplained) that many older adults, who died with complete cognitive integrity, were shown at autopsy to have massive amounts of amyloid plaques in their brains.  Evidence favoring amyloid location over amyloid burden in diagnosing Alzheimer's disease offers a potential explanation for these puzzling observations.

The amyloid hypothesis has evolved considerably since it was first introduced.  This research may offer a further refinement and a better understanding of the complex pathology of Alzheimer's Disease.

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