Alzheimer ' s Subtypes Differentiated by How and Why Amyloid- β Accumulates

The authors of this open access commentary paint a picture of Alzheimer's disease as a condition that starts in a variety of different ways, all of which lead to amyloid-β accumulation, and this is then the common gateway to pathology and dementia. Once an individual begins to accumulate raised levels of amyloid-β, then the characteristic degeneration of Alzheimer's proceeds from there. This is a slow burn over years or decades in which the biochemistry of the brain becomes ever more aberrant, culminating in the development of tau aggregates, inflammation, dementia, and cell death. The question has always been why only a fraction of people with any given risk factor go on to develop raised amyloid-β levels and full blown Alzheimer's disease. A variety of explanations are presently in various stages of construction and proof, most of which propose a way in which elevated amyloid-β levels might arise in only a portion of the population. Examples include persistent viral infection and differences in the drainage of cerebrospinal fluid through the cribriform plate. Postmortem data clearly shows that Alzheimer's disease (AD) pathology rarely occurs in isolation. Most AD patients harbor more than one pathology in the brain, with cerebrovascular disease being the most common coexisting pathology. Furthermore, the frequency of both cerebrovascular and Alzheimer's disease increases with age. However, in what way cerebrovascular disease and AD pathology act in syner...
Source: Fight Aging! - Category: Research Authors: Tags: Daily News Source Type: blogs