School of Biological Sciences, University of Queensland, Brisbane, 4072, Australia.
Centre of Excellence in Molecular Biology, University of the Punjab, Thokar Niaz Baig, Lahore, 54000, Pakistan.
J Biomed Sci. 2017 Sep 19;24(1):76. doi: 10.1186/s12929-017-0379-z.
Reactive oxidative species (ROS) toxicity remains an undisputed cause and link between Alzheimer's disease (AD) and Type-2 Diabetes Mellitus (T2DM). Patients with both AD and T2DM have damaged, oxidized DNA, RNA, protein and lipid products that can be used as possible disease progression markers. Although the oxidative stress has been anticipated as a main cause in promoting both AD and T2DM, multiple pathways could be involved in ROS production. The focus of this review is to summarize the mechanisms involved in ROS production and their possible association with AD and T2DM pathogenesis and progression. We have also highlighted the role of current treatments that can be linked with reduced oxidative stress and damage in AD and T2DM.
活性氧（ROS）毒性仍然是阿尔茨海默病（AD）和 2 型糖尿病（T2DM）之间不可争议的原因和联系。患有 AD 和 T2DM 的患者的 DNA、RNA、蛋白质和脂质产物都受到了损伤和氧化，这些产物可以作为可能的疾病进展标志物。尽管氧化应激被认为是促进 AD 和 T2DM 的主要原因，但可能有多种途径涉及 ROS 的产生。本综述的重点是总结 ROS 产生的机制及其与 AD 和 T2DM 发病机制和进展的可能关联。我们还强调了当前治疗方法的作用，这些方法可以与 AD 和 T2DM 中的氧化应激和损伤减少相关联。
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