Abnormal energy metabolism and tau phosphorylation in the brains of middle-aged mice in response to atmospheric PM2.5 exposure
Rui Gao , Tingting Ku , Xiaotong Ji , Yingying Zhang , Guangke Li , Nan Sang
DOI:10.1016/j.jes.2017.06.037
Received March 30, 2017,Revised June 28, 2017, Accepted June 29, 2017, Available online July 11, 2017
Volume 29,2017,Pages 145-153
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.
