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淀粉样蛋白、铝与阿尔茨海默病的病因学

Amyloid, aluminium and the aetiology of Alzheimer's disease.

作者信息

Storey E, Masters C L

机构信息

Department of Pathology, University of Melbourne, Parkville, VIC.

出版信息

Med J Aust. 1995 Sep 4;163(5):256-9. doi: 10.5694/j.1326-5377.1995.tb124564.x.

Abstract

Several lines of evidence suggest that neurotoxic beta A4 amyloid deposits are of prime importance in the pathogenesis of Alzheimer's disease. Epidemiologically determined risk factors such as Down's syndrome, head injury and apoE allelic status can be explained on the basis of this hypothesis. However, there are difficulties with the hypothesis--amyloid accumulation may be necessary, but is not sufficient to produce the neuronal damage seen in Alzheimer's disease. The association between aluminum exposure and Alzheimer's disease remains unproven and is considered to be increasingly peripheral to recent developments in our understanding of the disease.

摘要

多条证据表明,具有神经毒性的β淀粉样蛋白沉积物在阿尔茨海默病的发病机制中至关重要。基于这一假说,流行病学确定的风险因素,如唐氏综合征、头部损伤和载脂蛋白E等位基因状态,都可以得到解释。然而,该假说也存在一些问题——淀粉样蛋白的积累可能是必要的,但不足以产生阿尔茨海默病中所见的神经元损伤。铝暴露与阿尔茨海默病之间的关联尚未得到证实,并且在我们对该疾病的最新认识中,其重要性越来越低。

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