The present understanding of Alzheimer’s disease is illustrative of a broader issue with aging in general, in that while there is considerable evidence to pin down specific pathological mechanisms in cells and tissues, it is hard to prove exactly how these mechanisms interact. What is cause, what is consequence. What is important, what is merely a side-effect of other, important processes. At present there is some upheaval in the Alzheimer’s research community based on the failure of amyloid-β clearance to produce meaningful benefits in patients. This may or may not disrupt the present thinking on the condition, that early amyloid-β aggregation sets the stage for later neuroinflammation and tau aggregation. Amyloid-β may be a good early target, or it may turn out to be a side-effect of rising levels of chronic inflammation or persistent infection, and thus not a useful target at all.
Alzheimer’s disease (AD) is the most common neurodegenerative disorder seen in age-dependent dementia. There is currently no effective treatment for AD, which may be attributed in part to lack of a clear underlying mechanism. Studies within the last few decades provide growing evidence for a central role
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