Free radicals as mediators of toxicity in Alzheimer's disease: a review and hypothesis.
Free radicals as mediators of toxicity in Alzheimer's disease: a review and hypothesis.
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自由基作为阿尔茨海默病毒性介质：回顾和假设。
DOI：
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发表时间：
2000
期刊：
影响因子：
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通讯作者：
M. Orrell
中科院分区：
文献类型：
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作者：
N. Tabet;D. Mantle;M. Orrell
最近的研究越来越多地表明，自由基诱导的组织损伤在阿尔茨海默病(AD)的发病机制中起着核心作用。在这篇文章中，我们回顾了自由基与其他主要因素/代谢区域相互作用的证据，这些因素/代谢区域也与AD有关，包括β-淀粉样变性、炎性细胞因子、线粒体功能障碍和金属离子/同型半胱氨酸。我们假设，在AD的病因学和治疗中，不应单独考虑自由基和抗氧化剂。所有上述因素之间的相互诱导和自我放大的相互作用在本病的发病机制中起重要作用，并应针对其采取多种药物治疗策略。
Recent research has increasingly suggested a central role for free radical induced tissue damage in the pathogenesis of Alzheimer's disease (AD). In this paper we review evidence for the interaction between free radicals and other major factors/metabolic areas which have also been implicated in AD, including beta-amyloidosis, inflammatory cytokines, mitochondrial dysfunction and metal ions/homocysteine. We hypothesize that free radicals and antioxidants should not be considered in isolation in the aetiology and treatment of AD. It is the reciprocal induction and self-amplifying interplay between all of the above factors which is important in the pathogenesis of this disorder, and to which multi-pharmacological therapeutic strategies should be directed.