Cholesterol and pathological processes in Alzheimer's disease

Abstract

Fundamental questions on the pathogenesis of Alzheimer's disease (AD) are how nontoxic, soluble amyloid β‐protein (Aβ) is converted to its toxic, aggregated form and how functional tau is hyperphosphorylated to form neurofibrillary tangles. Growing evidence from recent biochemical and cell biological studies suggests that altered cholesterol metabolism in neurons may underlie such pathological processes. The possibility that cholesterol is a risk factor in the development of AD has also been supported by recent epidemiological studies. Based on this line of evidence, it is noteworthy to examine the potency of cholesterol‐lowering medicine and/or diet in suppressing the development or the progression of AD.