Wisniewski H M, Wen G Y
New York State Institute for Basic Research in Developmental Disabilities, Staten Island 10314.
Ciba Found Symp. 1992;169:142-54; discussion 154-64. doi: 10.1002/9780470514306.ch9.
The hypothesis that aluminium (Al) is a cause of (or a risk factor in) the development of beta-amyloid plaques and neurofibrillary tangles (NFT) and dementia in Alzheimer's disease (AD) is based on studies by Wisniewski et al, Klatzo et al and Terry & Peña in 1965 that showed that injection of experimental animals with Al compounds induces the formation of NFT. Other publications revealed that Al affects cognitive functions in experimental animals and humans undergoing dialysis for renal failure. Electron probe and laser microprobe mass analysis (LAMMA) studies have demonstrated the presence of Al in NFT and cores of amyloid stars and nuclei of neurons in AD patients. Other studies have indicated the association between amyotrophic lateral sclerosis/Guam parkinsonism-dementia complex and Al in the environment. A recent report suggests that the chelating agent desferrioxamine slows the rate of cognitive decline in AD patients. Extensive studies of the pathology of AD and Al-induced encephalopathy by our group and others indicate that Al does not cause Alzheimer's disease neuropathology. However, under certain conditions, cognition can be affected when Al enters the brain. Therefore, for individuals with renal failure or undergoing dialysis or individuals with a damaged blood-brain barrier, the intake of Al should be controlled.
铝（Al）是阿尔茨海默病（AD）中β-淀粉样蛋白斑块、神经原纤维缠结（NFT）形成及痴呆的病因（或风险因素）这一假说，基于1965年维斯涅夫斯基等人、克拉佐等人以及特里和佩尼亚的研究，这些研究表明给实验动物注射铝化合物会诱导NFT形成。其他出版物显示，铝会影响实验动物以及接受肾衰竭透析治疗的人类的认知功能。电子探针和激光微探针质谱分析（LAMMA）研究已证实AD患者的NFT、淀粉样蛋白星状体核心及神经元细胞核中存在铝。其他研究表明肌萎缩侧索硬化症/关岛帕金森病-痴呆综合征与环境中的铝之间存在关联。最近一份报告表明，螯合剂去铁胺可减缓AD患者认知能力下降的速度。我们团队及其他人员对AD和铝诱导的脑病病理学进行的广泛研究表明，铝不会导致阿尔茨海默病神经病理学改变。然而，在某些情况下，铝进入大脑时会影响认知。因此，对于肾衰竭患者、正在接受透析的患者或血脑屏障受损的个体，应控制铝的摄入量。
