The neurotoxicity of environmental aluminum is still an issue.

The neurotoxicity of environmental aluminum is still an issue.
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DOI:
10.1016/j.neuro.2010.05.009
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发表时间:
2010-09
期刊:
影响因子:
3.4
通讯作者:
Bondy SC
Bondy SC
中科院分区:
医学3区
文献类型:
--
作者:
Bondy SC

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长期暴露于低水平的铝盐的神经毒性的证据描述了使用动物模型与铝在低水平,反映了那些发现在一些供水。重点是铝在加速和促进脑老化的一些指标的特点的潜在作用。这些标志包括特定大脑区域出现过度炎症。铝盐可以增加脑内胶质细胞活化、炎性细胞因子和淀粉样前体蛋白的水平。正常的大脑老化和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。这些不是归因于明显的外源性刺激,可能反映了生物体免疫反应的寿命史。铝盐可能是这种明显的无诱因反应的一种微妙的促进剂。
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 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.
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