Abstract
Alzheimer's disease (AD) is the most common cause of dementia with no cure at present. Cholesterol metabolism is closely associated with AD at several stages. ACAT1 converts free cholesterol to cholesteryl esters, and plays important roles in cellular cholesterol homeostasis. Recent studies show that in a mouse model, blocking ACAT1 provides multiple beneficial effects on AD. Here we review the current evidence that implicates ACAT1 as a therapeutic target for AD. We also discuss the potential usage of various ACAT inhibitors currently available to treat AD.
Publication types
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Research Support, N.I.H., Extramural
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Review
MeSH terms
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Acetyl-CoA C-Acetyltransferase / antagonists & inhibitors*
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Acetyl-CoA C-Acetyltransferase / genetics
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Acetyl-CoA C-Acetyltransferase / metabolism
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Alzheimer Disease / drug therapy*
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Alzheimer Disease / genetics
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Alzheimer Disease / metabolism
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Animals
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Enzyme Inhibitors / chemistry
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Enzyme Inhibitors / pharmacology*
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Humans
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Mice
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Sterol O-Acyltransferase / antagonists & inhibitors*
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Sterol O-Acyltransferase / genetics
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Sterol O-Acyltransferase / metabolism
Substances
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Enzyme Inhibitors
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Sterol O-Acyltransferase
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sterol O-acyltransferase 1
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ACAT1 protein, human
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Acat1 protein, mouse
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Acetyl-CoA C-Acetyltransferase