ACAT as a drug target for Alzheimer's disease

被引：42

作者：

Huttunen, Henri J. ^{[1
]}

Kovacs, Dora M. ^{[1
]}

机构：

[1] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Genet & Aging Res Unit,Neurobiol Dis Lab,MIND, Boston, MA 02129 USA

来源：

NEURODEGENERATIVE DISEASES | 2008年 / 5卷 / 3-4期

关键词：

Alzheimer's disease; amyloid; cholesterol; lipids; endoplasmic; reticulum;

D O I：

10.1159/000113705

中图分类号：

R74 [神经病学与精神病学];

学科分类号：

摘要：

Accumulation of P-amyloid peptide (A beta) in the brain regions responsible for memory and cognitive functions is a neuropathological hallmark of Alzheimer's disease. Cholesterol may be involved in many aspects of A beta metabolism. It affects generation, aggregation and clearance of A beta in the brain. Not only the amount but also the distribution of cholesterol within cells appears to modulate A beta biogenesis. ACAT is an enzyme that regulates subcellular cholesterol distribution by converting membrane cholesterol to cholesteryl esters for storage and transport. We have used various cell- and animal based models to show that inhibition of ACAT strongly reduces A beta generation and protects from amyloid pathology. Here, we discuss data supporting ACAT inhibition as a strategy to treat Alzheimer's disease. Copyright (c) 2008 S. KargerAG, Basel.

引用

页码：212 / 214

页数：3

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