Department of Neurology, Nanjing First Hospital, Nanjing Medical University, Nanjing, Jiangsu Province, People's Republic of China.
Department of Neurology, Geriatric Hospital of Nanjing Medical University, Nanjing, Jiangsu Province, People's Republic of China.
J Alzheimers Dis. 2020;77(3):923-934. doi: 10.3233/JAD-200359.
As one of the most harmful air pollutants, fine particulate matter (PM2.5) has been implicated as a risk factor for multiple diseases, which has generated widespread public concern. Accordingly, a growing literature links PM2.5 exposure with Alzheimer's disease (AD). A critical gap in our understanding of the adverse effects of PM2.5 on AD is the mechanism triggered by PM2.5 that contributes to disease progression. Recent evidence has demonstrated that PM2.5 can activate NLRP3 inflammasome-mediated neuroinflammation. In this review, we highlight the novel evidence between PM2.5 exposure and AD incidence, which is collected and summarized from neuropathological, epidemiological, and neuroimaging studies to in-depth deciphering molecular mechanisms. First, neuropathological, epidemiological, and neuroimaging studies will be summarized. Then, the transport pathway for central nervous system delivery of PM2.5 will be presented. Finally, the role of NLRP3 inflammasome-mediated neuroinflammation in PM2.5 induced-effects on AD will be recapitulated.
作为最有害的空气污染物之一，细颗粒物（PM2.5）已被认为是多种疾病的风险因素，引起了广泛的公众关注。因此，越来越多的文献将 PM2.5 暴露与阿尔茨海默病（AD）联系起来。我们对 PM2.5 对 AD 的不良影响的理解存在一个关键的差距，即引发疾病进展的 PM2.5 触发的机制。最近的证据表明，PM2.5 可以激活 NLRP3 炎性小体介导的神经炎症。在这篇综述中，我们强调了 PM2.5 暴露与 AD 发病率之间的新证据，这些证据是从神经病理学、流行病学和神经影像学研究中收集和总结的，以深入解读分子机制。首先，将总结神经病理学、流行病学和神经影像学研究。然后，将介绍 PM2.5 向中枢神经系统输送的途径。最后，将综述 NLRP3 炎性小体介导的神经炎症在 PM2.5 诱导的 AD 中的作用。
