title: Inflammation, mitochondria, and the inhibition of adult neurogenesis.
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 interleukin-6, tumor necrosis factor-α, 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.
authors: Department of Anesthesia, Stanford University School of Medicine, Stanford, California 94305, USA.
authors: Ludmila A
authors: LA
authors: Voloboueva
authors: Rona G
authors: RG
authors: Giffard
mesh_terms: D053687:Adult Stem Cells / Q000378:metabolism* / Q000473:pathology; D000818:Animals; D006801:Humans; D007249:Inflammation / Q000503:physiopathology*; D008928:Mitochondria / Q000378:metabolism* / Q000473:pathology*; D009410:Nerve Degeneration / Q000503:physiopathology; D058953:Neural Stem Cells / Q000378:metabolism* / Q000473:pathology; D055495:Neurogenesis / Q000502:physiology*