Abnormal energy metabolism and tau phosphorylation in the brains of middle-aged mice in response to

• 作 者: Rui Gao Tingting Ku Xiaotong J
• 机 构: College of Environment and Resource, Research Center of Environment and Health, Shanxi University, T
• 出 处: 环境科学学报（英文版）
• 发表日期: 2017年12期
• 关键词: Fine particulate matter (PM2.5) Mitochondrial structure and function Energy meta

In light of the accelerated aging of the global population and the deterioration of the atmosphere pollution,we sought to clarify the potential mechanisms by which fine particulate matter (PM2.5) can cause cognitive impairment and neurodegeneration through the alteration of mitochondrial structure and function.The results indicate that PM2.5 inhalation reduces ATP production by disrupting the aerobic tricarboxylic acid cycle and oxidative phosphorylation,thereby causing the hypophosphorylation of tau in the cortices of middle-aged mice.Furthermore,excessive reactive oxygen species generation was involved in the impairment.Interestingly,these alterations were partially reversed after exposure to PM2.5 ended.These findings clarify the mechanism involved in mitochondrial abnormality-related neuropathological dysfunction in response to atmospheric PM2.5 inhalation and provide an optimistic sight for alleviating the adverse health outcomes in polluted areas.