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The role of mitochondrial defects and oxidative stress in Alzheimer's disease

机译:线粒体缺陷和氧化胁迫在阿尔茨海默病中的作用

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摘要

Alzheimer's disease (AD) is a complex, progressive, and irreversible neurodegenerative disorder. Recent reports suggest that it affects more than 36 million people worldwide and accounts 60-80% of all cases of dementia. It is characterised by aberrations of multiple interactive systems and pathways, which ultimately lead to memory loss and cognitive dysfunction. The exact mechanisms and initial triggering factors that underpin the known pathological defects in AD remain to be fully elucidated. In addition, an effective treatment strategy to reduce the progression of AD is yet to be achieved. In the light of above-mentioned facts, our article deals with the exploration of the mitochondrial defect and oxidative stress leading to this devastating disease. In this communication, we have highlighted specific mitochondrial and antioxidant-directed approach to ameliorate and manage AD. Nonetheless, new approaches should also be investigated that could tackle various molecular events involved in AD pathogenicity.
机译:阿尔茨海默病(AD)是一种复杂的,进行性和不可逆的神经变性障碍。最近的报告表明,它影响全世界3600多万人,占所有痴呆症病例的60-80%。它的特征在于多个交互式系统和途径,最终导致内存损失和认知功能障碍。在广告中施加已知病理缺陷的确切机制和初始触发因子仍然被完全阐明。此外,尚未实现减少广告进展的有效治疗策略。根据上述事实,我们的文章涉及探索线粒体缺陷和氧化应激,导致这种破坏性疾病。在这种沟通中,我们突出了特定的线粒体和抗氧化指导方法来改善和管理广告。尽管如此,还应调查新方法,这可以解决涉及AD致病性的各种分子事件。

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