Inflammation, mitochondria, and the inhibition of adult neurogenesis.
Inflammation, mitochondria, and the inhibition of adult neurogenesis.
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DOI：
10.1002/jnr.22768
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发表时间：
2011-12
影响因子：
4.2
通讯作者：
Giffard, Rona G.
中科院分区：
文献类型：
--
作者：
Voloboueva, Ludmila A.;Giffard, Rona G.
神经发生的过程贯穿整个生命，哺乳动物的大脑每天都会产生成千上万的新神经元。海马神经发生损伤被认为与神经退行性疾病有关，包括与衰老、阿尔茨海默病、帕金森病和电离辐射相关的认知能力下降。这些神经退行性疾病都以促炎改变和激活的小胶质细胞数量增加为特征。活化的小胶质细胞产生多种促炎因子，包括IL-6、TNF-α、活性氧和一氧化氮，它们都是抗神经原性的。这些相同的因素也被证明抑制线粒体功能，但线粒体在神经发生中的作用仍然很少被研究。这篇简短的综述总结了几项研究的发现，这些研究支持线粒体损伤作为炎症相关神经发生减少机制的一部分。
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 pro-inflammatory factors, including IL-6, TNF-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.
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影响因子：
2.7
作者：
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通讯作者：
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DOI：
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发表时间：
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影响因子：
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作者：
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