Abstract
Lipids play an important part as risk factors for Alzheimer’s disease. This article summarizes the current understanding of the molecular mechanism by which amyloid-β (Aβ) peptides regulate cholesterol and sphingomyelin metabolism, and how in return cholesterol and sphingomyelin regulate Aβ peptide production. An understanding of the physiological function of amyloid precursor protein processing and Aβ function is critical for the development of future therapeutic approaches, e.g. statin treatment.

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