Oxidative stress and mitochondrial damage are key factors in the development of neurodegenerative diseases such as Alzheimer's disease (AD), Parkinson's disease (PD), and amyotrophic lateral sclerosis (ALS). Oxidative stress results from the overproduction of reactive oxygen species (ROS), which can damage mitochondrial DNA, impair the mitochondrial respiratory chain, alter membrane permeability, and disrupt calcium homeostasis. These changes contribute to neuronal dysfunction and neurodegeneration. Mitochondrial dysfunction is a major trigger for these diseases, and strategies to modify mitochondrial dysfunction may offer therapeutic interventions. In AD, mitochondrial damage is associated with increased oxidative stress, leading to protein misfolding, amyloid plaque formation, and mitochondrial dysfunction. In PD, mitochondrial defects, such as mutations in mitochondrial DNA and complex I, are implicated in disease pathogenesis. In ALS, mitochondrial damage is linked to the accumulation of mutant superoxide dismutase 1 (SOD1), which impairs mitochondrial function and leads to neuronal death. Additionally, mitochondrial damage is a common feature in other neurodegenerative diseases, including Huntington's disease and Friedreich ataxia. Mitochondrial damage disrupts the mitochondrial defense system, leading to increased ROS production and further mitochondrial dysfunction. ROS can also disrupt calcium homeostasis, leading to mitochondrial permeability transition and neuronal death. Mitochondrial dysfunction is a central feature of neurodegenerative diseases, and targeting mitochondrial dysfunction may provide a promising approach for the prevention and treatment of these diseases.Oxidative stress and mitochondrial damage are key factors in the development of neurodegenerative diseases such as Alzheimer's disease (AD), Parkinson's disease (PD), and amyotrophic lateral sclerosis (ALS). Oxidative stress results from the overproduction of reactive oxygen species (ROS), which can damage mitochondrial DNA, impair the mitochondrial respiratory chain, alter membrane permeability, and disrupt calcium homeostasis. These changes contribute to neuronal dysfunction and neurodegeneration. Mitochondrial dysfunction is a major trigger for these diseases, and strategies to modify mitochondrial dysfunction may offer therapeutic interventions. In AD, mitochondrial damage is associated with increased oxidative stress, leading to protein misfolding, amyloid plaque formation, and mitochondrial dysfunction. In PD, mitochondrial defects, such as mutations in mitochondrial DNA and complex I, are implicated in disease pathogenesis. In ALS, mitochondrial damage is linked to the accumulation of mutant superoxide dismutase 1 (SOD1), which impairs mitochondrial function and leads to neuronal death. Additionally, mitochondrial damage is a common feature in other neurodegenerative diseases, including Huntington's disease and Friedreich ataxia. Mitochondrial damage disrupts the mitochondrial defense system, leading to increased ROS production and further mitochondrial dysfunction. ROS can also disrupt calcium homeostasis, leading to mitochondrial permeability transition and neuronal death. Mitochondrial dysfunction is a central feature of neurodegenerative diseases, and targeting mitochondrial dysfunction may provide a promising approach for the prevention and treatment of these diseases.