The amyloid hypothesis, which has dominated Alzheimer’s disease research, drug discovery, and clinical trial studies for more than 30 years, supposes that the accumulation of amyloid-β is the primary trigger for the eventual development of mild cognitive impairment and progression to dementia in Alzheimer’s disease. Indeed, the most recent treatments for Alzheimer’s disease target amyloid and appear to slow progression in some patients. Importantly, other downstream molecules and processes are known to contribute to the development of Alzheimer’s disease and should be considered critical mediators in disease progression.

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