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Various Markers

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ACAT as a Drug Target for Alzheimer’s Disease

Huttunen H.J. · Kovacs D.M.

Author affiliations

Neurobiology of Disease Laboratory, Genetics and Aging Research Unit, MassGeneral Institute for Neurodegenerative Disease (MIND), Massachusetts General Hospital, Harvard Medical School, Charlestown, Mass., USA

Corresponding Author

Dr. Dora M. Kovacs

Neurobiology of Disease Laboratory, Genetics and Aging Research Unit

Massachusetts General Hospital, Harvard Medical School

114 16th St., Charlestown, MA 02129 (USA)

Tel. +1 617 726 3668, Fax +1 617 724 1823, E-Mail Dora_Kovacs@hms.harvard.edu

Related Articles for ""

Neurodegenerative Dis 2008;5:212–214

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Accumulation of β-amyloid peptide (Aβ) 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 Aβmetabolism. It affects generation, aggregation and clearance of Aβin the brain. Not only the amount but also the distribution of cholesterol within cells appears to modulate Aβbiogenesis. 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 Aβgeneration and protects from amyloid pathology. Here, we discuss data supporting ACAT inhibition as a strategy to treat Alzheimer’s disease.

© 2008 S. Karger AG, Basel

Article / Publication Details

First-Page Preview
Abstract of Various Markers

Published online: March 06, 2008
Issue release date: March 2008

Number of Print Pages: 3
Number of Figures: 0
Number of Tables: 0

ISSN: 1660-2854 (Print)
eISSN: 1660-2862 (Online)

For additional information: http://www.karger.com/NDD

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