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.
View at publisher
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.).
209 downloads since deposited on 19 Oct 2009
8 downloads since 12 months
|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
|Dewey Decimal Classification:||570 Life sciences; biology
610 Medicine & health
|Deposited On:||19 Oct 2009 12:40|
|Last Modified:||05 Apr 2016 13:30|
|Additional Information:||The original publication is available at www.springerlink.com|
Users (please log in): suggest update or correction for this item
Repository Staff Only: item control page