Exposure to a real traffic environment impairs brain cognition in aged mice

Traffic-related air pollution (TRAP) has been a common public health problem, which is associated with central nervous system dysfunction according to large-scale epidemiological studies. Current studies are mostly limited to artificial laboratory exposure environments and specific genetic mechanisms remain unclear. Therefore, we chose a real-world transportation environment to expose aged mice, transporting them from the laboratory to a 1-m-high dry platform inside the campus and tunnel, and the mice were exposed daily from 7 a.m. to 7 p.m. for 2, 4 and 12 weeks respectively. Compared with the control group (in campus), the memory function of mice in the experimental group (in tunnel) was significantly impaired in the Morris water maze test. TRAP exposure increased the number of activated microglia in the hippocampal DG, CA1, CA3 regions and dorsolateral pre -frontal cortex (dPFC). And neuroinflammation and oxidative stress levels were up-regulated in both hippo-campus and dPFC of aged mice. By screening the risk genes of Alzheimer's disease, we found the mRNA and protein levels of ABCA7 were down-regulated and those of PYK2 were up-regulated. The DNA methylation ratios increased in four CpG sites of abca7 promoter region and decreased in one CpG site of pyk2 promoter region, which were consistent with the altered expression of ABCA7 and PYK2. In conclusion, exposure to the real traffic environment impaired memory function and enhanced neuroinflammation and oxidative stress responses, which could be relevant to the altered expression and DNA methylation levels of ABCA7 and PYK2. Our work provides a new and promising understanding of the pathological mechanisms of cognitive impairment caused by traffic-related air pollution.

Automated summary

Traffic-related air pollution impairs memory function and enhances neuroinflammation and oxidative stress responses, which may be associated with altered expression and DNA methylation levels of ABCA7 and PYK2.