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Permanent URL to this publication: http://dx.doi.org/10.5167/uzh-23236

Ogunshola, O O; Antoniou, X (2009). Contribution of hypoxia to Alzheimer's disease: is HIF-1alpha a mediator of neurodegeneration? Cellular and Molecular Life Sciences, 66(22):3555-3563.

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Abstract

The mammalian brain is extremely sensitive to alterations in cellular homeostasis as a result of environmental or physiological insults. In particular, hypoxic/ischemic challenges (i.e. reduced oxygen and/or glucose delivery) cause severe and detrimental alterations in brain function and can trigger neuronal cell death within minutes. Unfortunately, as we age, oxygen delivery to cells and tissues is impaired, thereby increasing the susceptibility of neurons to damage. Thus, hypoxic (neuronal) adaptation is significantly compromised during aging. Many neurological diseases, such as stroke, Alzheimer's disease (AD), Parkinson's disease and diabetes, are characterized by hypoxia, a state that is believed to only exacerbate disease progression. However, the contribution of hypoxia and hypoxia-mediated pathways to neurodegeneration remains unclear. This review discusses current evidence on the contribution of oxygen deprivation to AD, with an emphasis on hypoxia inducible transcription factor-1 (HIF-1)-mediated pathways and the association of AD with the cytoskeleton regulator cyclin-dependent kinase 5. (Part of a multi-author review.).

Item Type:Journal Article, refereed, further contribution
Communities & Collections:05 Vetsuisse Faculty > Institute of Veterinary Physiology
04 Faculty of Medicine > Center for Integrative Human Physiology
DDC:570 Life sciences; biology
610 Medicine & health
Language:English
Date:November 2009
Deposited On:19 Oct 2009 12:40
Last Modified:27 Nov 2013 20:14
Publisher:Springer
ISSN:1420-682X
Additional Information:The original publication is available at www.springerlink.com
Publisher DOI:10.1007/s00018-009-0141-0
PubMed ID:19763399
Citations:Web of Science®. Times Cited: 36
Google Scholar™
Scopus®. Citation Count: 38

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