Aluminium as a risk factor in Alzheimer's disease, with emphasis on drinking water

Aluminium as a risk factor in Alzheimer's disease, with emphasis on drinking water
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DOI:
10.1016/s0361-9230(01)00459-2
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发表时间:
2001-05-15
影响因子:
3.8
通讯作者:
Flaten, TP
Flaten, TP
中科院分区:
医学3区
文献类型:
--
作者:
Flaten, TP

文献摘要

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铝(Al)显然是一种强大的神经毒物。大量证据表明铝可能在阿尔茨海默病(AD)的病因学或发病机制中发挥作用,但这种联系是否是因果关系仍有待讨论。本文综述了有关铝和AD的流行病学证据。在已发表的13项关于饮用水中铝与AD的流行病学研究中,有9项显示出统计学上显著的正相关关系。鉴于难以产生高质量的数据,为AD的发生,也为铝暴露,与由此产生的不可避免的错误分类错误的任何真正的关联偏向零值,这些研究是非常一致的。在他们的解释的一个主要问题是,饮用水,即使在高铝浓度,只贡献了一小部分的总膳食摄入量的铝。特别是,经常消费者的抗酸剂摄入量的铝每天克,数千倍的量通过饮用水,和抗酸剂暴露和AD的流行病学研究已基本上是负面的。然而,铝在胃肠道中的吸收非常差,并且目前不能排除饮用水中存在的某些铝组分可能特别具有生物可利用性的可能性。将Al和AD联系起来的综合证据需要大量的研究工作。这些努力应侧重于阐明铝毒性的细胞和分子机制以及铝在人体内的基本代谢和动力学,并进一步开展流行病学研究,包括铝暴露的不同途径以及已知或怀疑影响个体对AD易感性的变量,如载脂蛋白E等位基因状态和AD家族史。(C)2001 Elsevier Science Inc.
Aluminium (Al) is clearly a powerful neurotoxicant. Considerable evidence exists that Al may play a role in the aetiology or pathogenesis of Alzheimer's disease (AD), but whether the link is causal is still open to debate. This paper reviews the epidemiological evidence linking Al and AD. Nine out of 13 published epidemiological studies of Al in drinking water and AD have shown statistically significant positive relations. Given the difficulty in producing high-quality data for the occurrence of AD and also for Al exposure, with the resulting unavoidable misclassification errors biasing any true association towards the null value, these studies are remarkably consistent. A major problem in their interpretation is that drinking water, even at high Al concentrations, only contributes a fraction of the total dietary intake of Al. In particular, regular consumers of antacids ingest gram amounts of Al daily, thousands of times the amounts taken in through drinking water, and epidemiological studies of antacid exposure and AD have been largely negative. However, Al is very poorly absorbed in the gastrointestinal tract, and the possibility that some Al fractions present in drinking water may be particularly bioavailable cannot be dismissed at present. The combined evidence linking Al and AD warrants substantial research efforts. Such efforts should focus on clarification of the cellular and molecular mechanisms in Al toxicity and of the basic metabolism and kinetics of Al in the human body, and on further epidemiological studies including diverse routes of Al exposure and also variables that are known or suspected to influence the individuals' susceptibility to AD, such as apolipoprotein E allele status and family history of AD. (C) 2001 Elsevier Science Inc.