Song Hyein, Lee Jiyong, Lee Yeeun, Kim Seungju, Kang Shinwoo
Department of Clinical Pharmacology, College of Medicine, Soonchunhyang University, 31, Soonchunhyang 6-gil, Dongnam-gu, Cheonan-si 31151, Chungcheongnam-do, Republic of Korea.
Int J Mol Sci. 2025 Apr 1;26(7):3272. doi: 10.3390/ijms26073272.
Chronic alcohol consumption leads to excessive production of reactive oxygen species (ROS), driving oxidative stress that contributes to both alcohol use disorder (AUD) and Alzheimer's disease (AD). This review explores how ROS-mediated mitochondrial dysfunction and neuroinflammation serve as shared pathological mechanisms linking these conditions. We highlight the role of alcohol-induced oxidative damage in exacerbating neurodegeneration and compare ROS-related pathways in AUD and AD. Finally, we discuss emerging therapeutic strategies, including mitochondrial antioxidants and inflammasome inhibitors, that target oxidative stress to mitigate neurodegeneration. Understanding these overlapping mechanisms may provide new insights for preventing and treating ROS-driven neurodegenerative disorders.
长期饮酒会导致活性氧(ROS)过度产生,引发氧化应激,这与酒精使用障碍(AUD)和阿尔茨海默病(AD)都有关联。本综述探讨了ROS介导的线粒体功能障碍和神经炎症如何作为连接这些病症的共同病理机制。我们强调了酒精诱导的氧化损伤在加剧神经退行性变中的作用,并比较了AUD和AD中与ROS相关的途径。最后,我们讨论了新兴的治疗策略,包括线粒体抗氧化剂和炎性小体抑制剂,这些策略以氧化应激为靶点来减轻神经退行性变。了解这些重叠机制可能为预防和治疗由ROS驱动的神经退行性疾病提供新的见解。