tailieunhanh - báo cáo hóa học: " Air pollution & the brain: Subchronic diesel exhaust exposure causes neuroinflammation and elevates early markers of neurodegenerative disease"

Tuyển tập báo cáo các nghiên cứu khoa học quốc tế ngành hóa học dành cho các bạn yêu hóa học tham khảo đề tài: Air pollution & the brain: Subchronic diesel exhaust exposure causes neuroinflammation and elevates early markers of neurodegenerative disease | Levesque et al. Journal of Neuroinflammation 2011 8 105 http content 8 1 105 JJOURNAL1 OF. NEUROINFLAMMATION RESEARCH Open Access Air pollution the brain Subchronic diesel exhaust exposure causes neuroinflammation and elevates early markers of neurodegenerative disease Shannon Levesque1 Michael J Surace1 Jacob McDonald2 and Michelle L Block1 Abstract Background Increasing evidence links diverse forms of air pollution to neuroinflammation and neuropathology in both human and animal models but the effects of long-term exposures are poorly understood. Objective We explored the central nervous system consequences of subchronic exposure to diesel exhaust DE and addressed the minimum levels necessary to elicit neuroinflammation and markers of early neuropathology. Methods Male Fischer 344 rats were exposed to DE 992 311 100 35 and 0 qg PM m3 by inhalation over 6 months. Results DE exposure resulted in elevated levels ofTNFa at high concentrations in all regions tested with the exception of the cerebellum. The midbrain region was the most sensitive where exposures as low as 100 qg PM m3 significantly increased brain TNFa levels. However this sensitivity to DE was not conferred to all markers of neuroinflammation as the midbrain showed no increase in IL-6 expression at any concentration tested an increase in IL-1Ị3 at only high concentrations and a decrease in MIP-1a expression supporting that compensatory mechanisms may occur with subchronic exposure. Ap42 levels were the highest in the frontal lobe of mice exposed to 992 qg PM m3 and tau pS199 levels were elevated at the higher DE concentrations 992 and 311 qg PM m3 in both the temporal lobe and frontal lobe indicating that proteins linked to preclinical Alzheimer s disease were affected. a Synuclein levels were elevated in the midbrain in response to the 992 qg PM m3 exposure supporting that air pollution may be associated with early Parkinson s disease-like pathology. Conclusions Together the