a Laboratory of Environmental Biomedicine, Hubei Key Laboratory of Genetic Regulation and Integrative Biology, College of Life Science , Central China Normal University , Wuhan , China.
b Department of Food Science and Engineering , Moutai College , Renhuai , China.
Toxicol Mech Methods. 2018 Feb;28(2):95-104. doi: 10.1080/15376516.2017.1368053. Epub 2017 Aug 29.
Alzheimer's disease (AD) is a serious, common, global disease, yet its etiology and pathogenesis are incompletely understood. Although an association between AD and exposure to air pollutants has been discussed, the effects of pollutants on the functioning of the brain remain unclear. The indoor environment is where exposure to formaldehyde (FA) can occur. Whether exposure to FA contributes to the development of AD needs to be investigated. To determine the objective, C57BL/6 mice were exposed daily to FA (0, 0.155, 1.55 and 15.5 mg/kg/day) for 1 week. After acute FA exposure, some early AD-like changes [cognitive deficits, pathological alterations in the mouse brain, accumulation of total β-amyloid plaques 1-42 (Aβ) and hyper-phosphorylated tau (Tau-P) in the cerebral cortex] were detected after exposure to high concentrations of FA (1.55 or 15.5 mg/kg/day). The permeability of the blood-brain barrier (BBB), activation of astrocyte and microglia, oxidative stress (OS) and inflammation were analyzed to explore the toxicity mechanisms behind the development of early AD-like changes. While exposed to a low concentration of FA (0.155 mg/kg/day) had little or no adverse effects on the mouse brain. The results indicated that acute FA exposure induced early AD-like changes in mouse brain, increased the susceptibility of AD in mouse.
阿尔茨海默病(AD)是一种严重的、常见的全球性疾病,但病因和发病机制尚不完全清楚。虽然 AD 与接触空气污染物之间存在关联,但污染物对大脑功能的影响仍不清楚。室内环境是接触甲醛(FA)的地方。FA 暴露是否会导致 AD 的发生尚需研究。为了确定目的,C57BL/6 小鼠每天暴露于 FA(0、0.155、1.55 和 15.5mg/kg/天)1 周。在急性 FA 暴露后,在高浓度 FA(1.55 或 15.5mg/kg/天)暴露后,检测到一些早期 AD 样变化[认知缺陷、小鼠大脑的病理改变、总β-淀粉样蛋白斑块 1-42(Aβ)和磷酸化 tau(Tau-P)在大脑皮层中的积累]。分析血脑屏障(BBB)通透性、星形胶质细胞和小胶质细胞激活、氧化应激(OS)和炎症,以探讨早期 AD 样变化发展背后的毒性机制。而暴露于低浓度 FA(0.155mg/kg/天)对小鼠大脑几乎没有或没有不良影响。结果表明,急性 FA 暴露诱导了小鼠大脑的早期 AD 样变化,增加了小鼠患 AD 的易感性。