Bilski Rafał, Dąbkowski Stanisław, Kozieł Igor, Kozicki Michał, Małachowska Anna, Przygocki Mikołaj, Tyska Oliwia
Department of Medical Biology and Biochemistry, Faculty of Medicine, Ludwik Rydygier Collegium Medicum in Bydgoszcz, Nicolaus Copernicus University in Toruń, 24 Karłowicza St., 85-092 Bydgoszcz, Poland.
Students Research Club of Medical Biology, Department of Medical Biology and Biochemistry, Faculty of Medicine, Ludwik Rydygier Collegium Medicum in Bydgoszcz, Nicolaus Copernicus University in Toruń, 87-100 Torun, Poland.
Biomolecules. 2025 Sep 19;15(9):1345. doi: 10.3390/biom15091345.
Alzheimer's disease (AD) is a progressive neurodegenerative disorder and one of the most pressing global health challenges. Increasing evidence highlights oxidative stress as a key factor in its pathogenesis, contributing to amyloid-β accumulation, tau hyperphosphorylation, neuroinflammation, and mitochondrial dysfunction. Oxidative stress markers, detected in the bodily fluids of AD patients, are considered promising diagnostic and prognostic tools. Despite extensive research, currently available therapies remain largely symptomatic, which emphasizes the need to develop novel, disease-modifying strategies. The aim of this review is to summarize current knowledge on the role of oxidative stress in the pathogenesis of AD and to evaluate therapeutic approaches aimed at its reduction. We discuss molecular mechanisms linking reactive oxygen species to neurodegeneration and present pharmacological strategies such as monoamine oxidase inhibitors and multifunctional agents, as well as natural antioxidants, dietary interventions, and novel therapeutic technologies. We pay particular attention to their efficacy, limitations, and translational challenges. A more profound understanding of oxidative stress-related mechanisms may facilitate the development of combined antioxidant, anti-inflammatory, and neuroprotective approaches, offering new perspectives for delaying disease progression and improving patient outcomes.
阿尔茨海默病(AD)是一种进行性神经退行性疾病,也是全球最紧迫的健康挑战之一。越来越多的证据表明氧化应激是其发病机制中的关键因素,导致淀粉样β蛋白积累、tau蛋白过度磷酸化、神经炎症和线粒体功能障碍。在AD患者体液中检测到的氧化应激标志物被认为是很有前景的诊断和预后工具。尽管进行了广泛研究,但目前可用的治疗方法大多只是对症治疗,这凸显了开发新型疾病修饰策略的必要性。本综述的目的是总结当前关于氧化应激在AD发病机制中的作用的知识,并评估旨在降低氧化应激的治疗方法。我们讨论了将活性氧与神经退行性变联系起来的分子机制,并介绍了诸如单胺氧化酶抑制剂和多功能药物等药理学策略,以及天然抗氧化剂、饮食干预和新型治疗技术。我们特别关注它们的疗效、局限性和转化挑战。对氧化应激相关机制的更深入理解可能有助于开发联合抗氧化、抗炎和神经保护方法,为延缓疾病进展和改善患者预后提供新的视角。