The puzzle of Alzheimer’s disease is why it only occurs in some people. Unlike other common age-related diseases, such as atherosclerosis, it isn’t universal, even in groups exhibiting all of the lifestyle risk factors. Thus a strong theme in the Alzheimer’s research community is the search for clear and robust differences in cellular biochemistry between people with and without the condition, in an attempt to shed more light on how and why Alzheimer’s arises.
In the absence of a complete understanding of how and why Alzheimer’s disease begins, the strategy for developing effective therapies is haphazard. Perhaps the obvious points of intervention based on today’s knowledge are good, perhaps not. The history of this research and development is not encouraging. Most past work has focused on clearance of amyloid-β aggregates, an obvious point of difference between diseased and normal brains, informed by the amyloid cascade hypothesis. Unfortunately, lowering amyloid-β levels in the brain has failed to produce improvements in patients.
Back to the question of why only some people suffer Alzheimer’s disease: a good deal of theorizing has taken place to try to explain this observation. For example, perhaps Alzheimer’s disease is primarily driven
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