Free radicals as mediators of toxicity in Alzheimer's disease: a review and hypothesis.

N Tabet, D Mantle, M Orrell
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Abstract

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.

自由基作为阿尔茨海默病毒性介质:综述与假设。
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。在本文中,我们回顾了自由基与其他主要因素/代谢区域之间相互作用的证据,这些因素/代谢区域也与AD有关,包括β -淀粉样变性,炎症细胞因子,线粒体功能障碍和金属离子/同型半胱氨酸。我们假设自由基和抗氧化剂不应该在AD的病因和治疗中单独考虑。上述所有因素之间的相互诱导和自我放大的相互作用在这种疾病的发病机制中是重要的,应该针对这些因素采取多种药物治疗策略。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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