Mitochondria are critical in ensuring cellular energy homeostasis and controlling vital processes like apoptosis, calcium signaling, and management of oxidative stress. Mitochondrial dynamics through ongoing fission, fusion, transport, and quality control are crucial for the maintenance of mitochondrial function and adjusting to cellular needs. Mitochondrial dynamics dysregulation has come to be a key characteristic of brain aging and neurodegenerative diseases. Aging is correlated with disturbed mitochondrial fission and fusion equilibrium, resulting in abnormal mitophagy, the presence of dysfunctional mitochondria, and augmented oxidative stress, further promoting neuronal impairment. The brain is most susceptible to mitochondrial dysfunction owing to considerable energy requirements and susceptibility to reactive oxygen species (ROS). Mitochondrial fragmentation, disrupted biogenesis, and abnormal axonal transport add to synaptic dysfunction and neuronal survival. New evidence highlights the importance of mitochondrial quality control mechanisms, such as mitophagy and biogenesis, in maintaining resistance to age-related damage and neuronal integrity. Genetic and epigenetic alterations also modulate the crucial proteins governing mitochondrial dynamics and steer the neurodegeneration course. Deciphering the association of brain aging and mitochondrial dynamics reveals insight into treatment modalities to attain mitochondrial homeostasis and avoid neuronal demise. The following chapter deals with the basic mechanisms governing mitochondrial dynamics, their importance in brain aging, and treatment modalities for targeting mitochondrial malfunction to avert cognitive impairment during aging.