铝与阿尔茨海默病:可能的致病机制综述。

R A Armstrong, S J Winsper, J A Blair
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引用次数: 62

摘要

慢性暴露于铝(Al)仍然是一个有争议的散发性阿尔茨海默病(AD)的可能原因。本文综述了Al一旦进入大脑和单个脑细胞,可能参与三个病理过程的证据:(1)产生异常形式的tau,导致细胞神经原纤维缠结和神经丝的形成;(2)淀粉样蛋白前体蛋白的加工,导致β -淀粉样蛋白沉积和老年斑的形成;(3)通过相互组织相容性系统,Al可能参与了AD患者免疫应答的启动。尽管最近有证据表明阿尔茨海默病可能参与了这些过程,但暴露于阿尔茨海默病中启动原发性病理过程的结论性案例仍有待建立。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Aluminium and Alzheimer's disease: review of possible pathogenic mechanisms.

Chronic exposure to aluminium (Al) remains a controversial possible cause of sporadic forms of Alzheimer's disease (AD). This article reviews the evidence that once Al enters the brain and individual brain cells, it may be involved in three pathological processes: (1) the production of abnormal forms of tau leading to the formation of cellular neurofibrillary tangles and neuropil threads; (2) the processing of the amyloid precursor protein, resulting in the formation of beta-amyloid deposits and senile plaques, and (3) that via the mutual histocompatibility system, Al could be involved in the initiation of the immune response observed in AD patients. Despite recent evidence that Al could be involved in these processes, a conclusive case that exposure to Al initiates the primary pathological process in sporadic AD remains to be established.

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