Current thinking on the mechanistic basis of Alzheimer's and implications for drug development

Alzheimer disease (AD) is the most common cause of dementia and is characterized by the aggregation and accumulation of two proteins in the brain, amyloid‐β (Aβ) and tau. Aβ and tau begin to buildup 15‐20 years before the clinical onset of AD dementia. Increasing evidence suggests that preventing or decreasing the amount of aggregated forms of both Aβ and tau in the brain can serve as potential disease‐modifying treatments for AD.