## Abstract Any pathological perturbation to the brain provokes a cascade of molecular and cellular events, which manifests in the form of microglial activation and release of various proinflammatory molecules. This eventually culminates in a profound neuroinflammatory reaction that characterizes t
Inflammation, mitochondria, and the inhibition of adult neurogenesis
β Scribed by Ludmila A. Voloboueva; Rona G. Giffard
- Publisher
- John Wiley and Sons
- Year
- 2011
- Tongue
- English
- Weight
- 466 KB
- Volume
- 89
- Category
- Article
- ISSN
- 0360-4012
No coin nor oath required. For personal study only.
β¦ Synopsis
Abstract
The process of neurogenesis continues throughout life, with thousands of new neurons generated every day in the mammalian brain. Impairment of hippocampal neurogenesis has been suggested to be involved in neurodegenerative conditions, including the cognitive decline associated with aging, Alzheimer's disease, Parkinson's disease, and ionizing radiation. These neurodegenerative conditions are all characterized by proinflammatory changes and increased numbers of activated microglia. Activated microglia produce a variety of proinflammatory factors, including interleukinβ6, tumor necrosis factorβΞ±, reactive oxygen species, and nitric oxide, all of which are antineurogenic. These same factors have also been shown to suppress mitochondrial function, but the role of mitochondria in neurogenesis remains barely investigated. This brief review summarizes the findings of several studies that support a role for mitochondrial impairment as part of the mechanism of the reduction of neurogenesis associated with inflammation. Β© 2011 WileyβLiss, Inc.
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