Oxidative Stress and the Role of Immune Cells in Alzheimer's Disease: Therapeutic Implications and Future Perspectives.

Nidhi Puranik, Minseok Song
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Abstract

The most common neurodegenerative illness and leading cause of death in the world is Alzheimer's disease (AD), which is extremely expensive to treat. None of the AD treatments that are currently in the market with approval have any effect on disease progression. However, numerous clinical studies aimed at reducing amyloid beta (Aβ) plaque development, boosting Aβ clearance, or reducing neurofibrillary tangle (NFT) failed or had conflicting results. As oxidative stress (OS), mitochondrial dysfunction, and chronic neuroinflammation are implicated in numerous interconnected vicious cascades, research has revealed new therapeutic targets, including enhancing mitochondrial bioenergetics and quality control, reducing oxidative stress, or modulating neuroinflammatory pathways. This review examines the role of oxidative stress (OS), mitochondrial dysfunction, neuroinflammation, and the interplay between peripheral and central immune systems in the pathogenesis of AD. We highlight how OS and immune dysregulation drive chronic neuroinflammation, exacerbating AD progression. Immune cells and inflammatory molecules emerge as critical players in disease pathology. Overall, this review concludes that targeting OS and immune system crosstalk represents promising therapeutic strategies for mitigating AD progression, providing a foundation for future interventions.

氧化应激和免疫细胞在阿尔茨海默病中的作用:治疗意义和未来展望。
世界上最常见的神经退行性疾病和主要死亡原因是阿尔茨海默病(AD),治疗费用极其昂贵。目前在市场上获得批准的阿尔茨海默病治疗方法都没有对疾病进展产生任何影响。然而,许多旨在减少淀粉样蛋白(Aβ)斑块形成、促进Aβ清除或减少神经原纤维缠结(NFT)的临床研究失败或结果相互矛盾。由于氧化应激(OS)、线粒体功能障碍和慢性神经炎症涉及许多相互关联的恶性级联反应,研究揭示了新的治疗靶点,包括增强线粒体生物能量和质量控制、减少氧化应激或调节神经炎症途径。本文综述了氧化应激(OS)、线粒体功能障碍、神经炎症以及外周和中枢免疫系统之间的相互作用在AD发病机制中的作用。我们强调OS和免疫失调如何驱动慢性神经炎症,加剧AD的进展。免疫细胞和炎症分子在疾病病理中扮演着关键角色。总的来说,本综述得出结论,靶向OS和免疫系统串扰是缓解AD进展的有希望的治疗策略,为未来的干预提供了基础。
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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