Mitochondrial dysfunction and reactive oxygen species (ROS) play critical roles in the pathogenesis of neurodegenerative diseases such as Alzheimer’s disease (AD) and Parkinson’s disease (PD). Mitochondria regulate energy production, redox homeostasis, and cellular signaling, and their dysfunction leads to oxidative stress, mitochondrial fragmentation, and impaired function. Mitochondrial dynamics, including fusion, fission, biogenesis, and mitophagy, are tightly regulated to maintain mitochondrial health. Dysregulation of these processes contributes to neurodegeneration. ROS, generated during mitochondrial respiration, can cause oxidative damage to cellular components, including proteins, lipids, and DNA, and promote inflammation. Mitochondrial dysfunction is implicated in the progression of AD and PD, with evidence showing that impaired mitochondrial function and excessive ROS production are key factors in disease development. Mitochondrial-targeted therapies, such as fusion and biogenesis enhancers, fission inhibitors, and antioxidants, are emerging as potential treatments for these diseases. Mitochondrial dysfunction also contributes to neuroinflammation through pathways like the cGAS–STING and NLRP3 inflammasome signaling. Targeting mitochondrial dysfunction and ROS is a promising strategy for developing novel therapies for neurodegenerative diseases.Mitochondrial dysfunction and reactive oxygen species (ROS) play critical roles in the pathogenesis of neurodegenerative diseases such as Alzheimer’s disease (AD) and Parkinson’s disease (PD). Mitochondria regulate energy production, redox homeostasis, and cellular signaling, and their dysfunction leads to oxidative stress, mitochondrial fragmentation, and impaired function. Mitochondrial dynamics, including fusion, fission, biogenesis, and mitophagy, are tightly regulated to maintain mitochondrial health. Dysregulation of these processes contributes to neurodegeneration. ROS, generated during mitochondrial respiration, can cause oxidative damage to cellular components, including proteins, lipids, and DNA, and promote inflammation. Mitochondrial dysfunction is implicated in the progression of AD and PD, with evidence showing that impaired mitochondrial function and excessive ROS production are key factors in disease development. Mitochondrial-targeted therapies, such as fusion and biogenesis enhancers, fission inhibitors, and antioxidants, are emerging as potential treatments for these diseases. Mitochondrial dysfunction also contributes to neuroinflammation through pathways like the cGAS–STING and NLRP3 inflammasome signaling. Targeting mitochondrial dysfunction and ROS is a promising strategy for developing novel therapies for neurodegenerative diseases.