Targeting Mitochondrial Dysfunction and Reactive Oxygen Species for Neurodegenerative Disease Treatment

Targeting Mitochondrial Dysfunction and Reactive Oxygen Species for Neurodegenerative Disease Treatment

2024 | Eui-Hwan Choi, Mi-Hye Kim and Sun-Ji Park
Alzheimer's disease (AD) and Parkinson's disease (PD) are the most common neurodegenerative diseases, affecting millions worldwide, particularly older individuals. Emerging evidence suggests that mitochondrial dysfunction and reactive oxygen species (ROS) generation play central roles in the onset and progression of these diseases. Mitochondria regulate respiratory function, ATP production, and cellular redox homeostasis, which are essential for cell survival. The balance among mitochondrial fission, fusion, biogenesis, and mitophagy is crucial for maintaining mitochondrial function. This review highlights recent progress in understanding the critical roles of ROS-induced oxidative stress, dysregulated mitochondrial dynamics, mitochondrial apoptosis, mitochondria-associated inflammation, and impaired mitochondrial function in the pathogenesis of AD and PD. It also discusses potential novel drugs, including mitochondrial fusion and biogenesis enhancers, mitochondrial fission inhibitors, and mitochondria-targeted antioxidants, as promising therapeutic strategies for treating these diseases.Alzheimer's disease (AD) and Parkinson's disease (PD) are the most common neurodegenerative diseases, affecting millions worldwide, particularly older individuals. Emerging evidence suggests that mitochondrial dysfunction and reactive oxygen species (ROS) generation play central roles in the onset and progression of these diseases. Mitochondria regulate respiratory function, ATP production, and cellular redox homeostasis, which are essential for cell survival. The balance among mitochondrial fission, fusion, biogenesis, and mitophagy is crucial for maintaining mitochondrial function. This review highlights recent progress in understanding the critical roles of ROS-induced oxidative stress, dysregulated mitochondrial dynamics, mitochondrial apoptosis, mitochondria-associated inflammation, and impaired mitochondrial function in the pathogenesis of AD and PD. It also discusses potential novel drugs, including mitochondrial fusion and biogenesis enhancers, mitochondrial fission inhibitors, and mitochondria-targeted antioxidants, as promising therapeutic strategies for treating these diseases.
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