Bir Aritri, Ghosh Arindam, Chauhan Aman, Saha Sarama, Saini Adesh K, Bisaglia Marco, Chakrabarti Sasanka
Department of Biochemistry, Dr B. C. Roy Multi-Speciality Medical Research Centre, Indian Institute of Technology Kharagpur, Kharagpur 721302, West Bengal, India.
Department of Biochemistry and Central Research Cell, Maharishi Markandeshwar Institute of Medical Sciences and Research, Maharishi Markandeshwar (Deemed to be University), Mullana-Ambala 133207, Haryana, India.
Antioxidants (Basel). 2024 Mar 5;13(3):316. doi: 10.3390/antiox13030316.
Oxidative burden plays a central role in Alzheimer's disease (AD) pathology, fostering protein aggregation, inflammation, mitochondrial impairment, and cellular dysfunction that collectively lead to neuronal injury. The role of exosomes in propagating the pathology of neurodegenerative diseases including AD is now well established. However, recent studies have also shown that exosomes are crucial responders to oxidative stress in different tissues. Thus, this offers new insights and mechanistic links within the complex pathogenesis of AD through the involvement of oxidative stress and exosomes. Several studies have indicated that exosomes, acting as intracellular communicators, disseminate oxidatively modified contents from one cell to another, propagating the pathology of AD. Another emerging aspect is the exosome-mediated inhibition of ferroptosis in multiple tissues under different conditions which may have a role in neurodegenerative diseases as well. Apart from their involvement in the pathogenesis of AD, exosomes enter the bloodstream serving as novel noninvasive biomarkers for AD; some of the exosome contents also reflect the cerebral oxidative stress in this disease condition. This review highlights the intricate interplay between oxidative stress and exosome dynamics and underscores the potential of exosomes as a novel tool in AD diagnosis.
氧化应激在阿尔茨海默病(AD)病理过程中起着核心作用,促进蛋白质聚集、炎症反应、线粒体损伤以及细胞功能障碍,这些共同导致神经元损伤。外泌体在包括AD在内的神经退行性疾病病理传播中的作用现已得到充分证实。然而,最近的研究也表明,外泌体是不同组织中氧化应激的关键响应者。因此,通过氧化应激和外泌体的参与,这为AD复杂的发病机制提供了新的见解和机制联系。多项研究表明,作为细胞内通讯者的外泌体将氧化修饰的物质从一个细胞传播到另一个细胞,从而传播AD的病理过程。另一个新出现的方面是外泌体在不同条件下对多种组织中铁死亡的抑制作用,这在神经退行性疾病中可能也发挥着作用。除了参与AD的发病机制外,外泌体进入血液循环,成为AD新型的非侵入性生物标志物;一些外泌体内容物也反映了这种疾病状态下的脑氧化应激。本综述强调了氧化应激与外泌体动态之间的复杂相互作用,并强调了外泌体作为AD诊断新工具的潜力。