Program in Environmental Toxicology, Division Occupational and Environmental Health, Department of Medicine, University of California, Irvine, CA 92697-1825, USA.
Neurotoxicology. 2010 Sep;31(5):575-81. doi: 10.1016/j.neuro.2010.05.009. Epub 2010 May 27.
Evidence for the neurotoxicity of extended exposure to low levels of aluminum salts is described using an animal model treated with aluminum at low levels reflecting those found in some water supplies. Emphasis is given to the potential role of aluminum in acceleration and promotion of some indices characteristic of brain aging. These hallmarks include the appearance of excess levels of inflammation in specific brain areas. Aluminum salts can increase levels of glial activation, inflammatory cytokines and amyloid precursor protein within the brain. Both normal brain aging and to a greater extent, Alzheimer's disease are associated with elevated basal levels of markers for inflammation. These are not attributable to obvious exogenous stimuli and may reflect the lifespan history of the organism's immune responses. It is possible that aluminum salts can act as a subtle promoter of such apparently unprovoked responses.
使用动物模型研究了低水平暴露于铝盐的神经毒性，该模型用的是反映某些供水中存在的铝水平的低剂量铝进行处理。本文重点介绍了铝在加速和促进一些与大脑衰老相关的指标方面的潜在作用。这些特征包括在特定脑区出现炎症水平升高。铝盐可增加大脑中神经胶质细胞激活、炎症细胞因子和淀粉样前体蛋白的水平。正常的大脑衰老，以及在更大程度上的阿尔茨海默病，都与炎症标志物的基础水平升高有关。这些升高不是由明显的外源性刺激引起的，可能反映了机体免疫反应的寿命史。铝盐可能会以一种微妙的方式促进这种看似无端的反应。
