作者: Carmen Vida , Eva M Gonzalez , Monica De la Fuente
DOI: 10.2174/1381612820666140130201734
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摘要: According to the oxidation-inflammation theory of aging, chronic oxidative stress and inflammatory situations (with higher levels oxidant compounds lower antioxidant anti-inflammatory defenses) are basis agerelated impairment organism functions, including those nervous immune systems, as well neuroimmune communication, which explains altered homeostasis resulting increase morbidity mortality. Overproduction can induce an response, since oxidants inflammation effectors. Thus, oxidation interlinked processes have many feedback loops. However, nature their potential interactions, mainly in brain cells, key involvement aging remain unclear. Moreover, context it has been described that oxidative-inflammatory situation occurs subjects with anxiety, this contributes immunosenescence, alteration survival responses shorter life span. As example this, a model premature mice, animals show poor response high cells tissues, immunosenescence expectancy, will be commented present review. This supports hypothesis anxiety inflammation, especially accelerates rate aging.