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ISSN: 2153-0637

Journal of Glycomics & Lipidomics
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Review Article

HemeOxygenase-1: Transducer of Sterol Dys-Regulation in Alzheimer Disease

Hascalovici J and Schipper HM*

Department of Neurology and Neurosurgery, McGill University, and Lady Davis Institute for Medical Research, Jewish General Hospital, Canada

*Corresponding Author:
Schipper HM
Lady Davis Institute for Medical Research
Jewish General Hospital, 3755 Cote Ste. Catherine Road
Montreal,Quebec H3T 1E2, Canada
Tel: 514-340-8260 Ext: 5588
Fax: 514-340-7502
E-mail: [email protected]

Received date: September 29, 2014; Accepted date: October 17, 2014; Published date: October 20, 2014

Citation: Hascalovici J, Schipper HM (2014) HemeOxygenase-1: Transducer of Sterol Dys-Regulation in Alzheimer Disease. J Glycomics Lipidomics 4:124. doi: 10.4172/2153-0637.1000124

Copyright: © 2014 Hascalovici J, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Cholesterol (CH) and oxysterols have been consistently implicated in brain aging, Alzheimer’s disease (AD) and otherhuman neurodegenerative conditions, althoughthe mechanisms underlying these relationships remain poorly understood. Heme oxygenase-1 (HO-1) is a highly-inducible stress protein responsible for the catabolism of heme to free iron, carbon monoxide (CO) and biliverdin/bilirubin. HO-1 mRNA and protein levels are augmented in Alzheimer-diseased neural tissues where they may promote pathological iron deposition and oxidative mitochondrial damage characteristic of this disorder. Here, we review evidence derived from cultured rat astroglia, post-mortem human AD brain samples, novel GFAP. HMOX1 transgenic mice and a triple transgenic AD mouse model (3xTg-AD) implicating HO-1 as a pivotal transducer of noxious ambient stimuli into abnormal patterns of brain sterol/oxysterol homeostasis germane to the pathogenesis of AD and other aging-related neurodegenerative disorders.

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