Yegambaram Manivannan, Manivannan Bhagyashree, Beach Thomas G, Halden Rolf U
Center for Environmental Security, The Biodesign Institute, Arizona State University, PO Box 875904 Tempe, AZ 85287, USA.
Curr Alzheimer Res. 2015;12(2):116-46. doi: 10.2174/1567205012666150204121719.
Alzheimer's dis ease (AD) is a leading cause of mortality in the developed world with 70% risk attributable to genetics. The remaining 30% of AD risk is hypothesized to include environmental factors and human lifestyle patterns. Environmental factors possibly include inorganic and organic hazards, exposure to toxic metals (aluminium, copper), pesticides (organochlorine and organophosphate insecticides), industrial chemicals (flame retardants) and air pollutants (particulate matter). Long term exposures to these environmental contaminants together with bioaccumulation over an individual's life-time are speculated to induce neuroinflammation and neuropathology paving the way for developing AD. Epidemiologic associations between environmental contaminant exposures and AD are still limited. However, many in vitro and animal studies have identified toxic effects of environmental contaminants at the cellular level, revealing alterations of pathways and metabolisms associated with AD that warrant further investigations. This review provides an overview of in vitro, animal and epidemiological studies on the etiology of AD, highlighting available data supportive of the long hypothesized link between toxic environmental exposures and development of AD pathology.
阿尔茨海默病（AD）是发达国家主要的死亡原因之一，70%的发病风险归因于遗传因素。其余30%的AD发病风险据推测包括环境因素和人类生活方式。环境因素可能包括无机和有机危害物、接触有毒金属（铝、铜）、农药（有机氯和有机磷杀虫剂）、工业化学品（阻燃剂）和空气污染物（颗粒物）。长期接触这些环境污染物以及个体一生中的生物累积被推测会诱发神经炎症和神经病理学变化，为AD的发展铺平道路。环境污染物暴露与AD之间的流行病学关联仍然有限。然而，许多体外和动物研究已经在细胞水平上确定了环境污染物的毒性作用，揭示了与AD相关的信号通路和代谢变化，值得进一步研究。本综述概述了关于AD病因的体外、动物和流行病学研究，强调了现有数据支持长期以来所假设的有毒环境暴露与AD病理发展之间的联系。
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