Mitochondria are essential for neuronal function, providing ATP and regulating Ca²+ and redox signaling. They play critical roles in synaptic plasticity, developmental processes, and neuronal survival. Mitochondrial dysfunction contributes to neurological disorders such as Alzheimer's, Parkinson's, and Huntington's disease, as well as stroke and psychiatric conditions. Mitochondria regulate Ca²+ homeostasis, energy metabolism, and apoptosis, and their dysfunction leads to oxidative stress, disrupted signaling, and cell death. Mitochondria are dynamic organelles that undergo fission and fusion, regulated by proteins like Drp1 and Mfn1/Mfn2. These processes are crucial for maintaining mitochondrial function and distribution within neurons. Mitochondrial transport along microtubules is mediated by motor proteins, and their movement is influenced by neuronal activity and energy demands. During development, mitochondria support neuronal differentiation and axonogenesis, and their distribution is critical for establishing neuronal polarity. Mitochondrial dysfunction can impair synaptic plasticity, leading to learning and memory deficits. Mitochondria also play a role in synaptic transmission by buffering Ca²+ and providing ATP. In neuronal cell death, mitochondria are involved in both necrosis and apoptosis. Necrosis occurs under severe energy deprivation and oxidative stress, while apoptosis is a programmed process involving mitochondrial permeability transition pores (PTP), cytochrome c release, and caspase activation. Mitochondrial dysfunction can lead to caspase-independent cell death (CIPCD), where AIF is released instead of cytochrome c. Mitochondria are also involved in neurodegenerative diseases, such as Alzheimer's, where amyloid-beta (Aβ) accumulation leads to oxidative stress and Ca²+ dysregulation. Mitochondrial dysfunction in these diseases is associated with impaired energy production, increased ROS, and disrupted Ca²+ homeostasis. Understanding mitochondrial biology and its role in neuronal function and disease is crucial for developing therapeutic strategies to prevent and treat neurological disorders. Advances in mitochondrial research are leading to new approaches for neuroprotection and regeneration.Mitochondria are essential for neuronal function, providing ATP and regulating Ca²+ and redox signaling. They play critical roles in synaptic plasticity, developmental processes, and neuronal survival. Mitochondrial dysfunction contributes to neurological disorders such as Alzheimer's, Parkinson's, and Huntington's disease, as well as stroke and psychiatric conditions. Mitochondria regulate Ca²+ homeostasis, energy metabolism, and apoptosis, and their dysfunction leads to oxidative stress, disrupted signaling, and cell death. Mitochondria are dynamic organelles that undergo fission and fusion, regulated by proteins like Drp1 and Mfn1/Mfn2. These processes are crucial for maintaining mitochondrial function and distribution within neurons. Mitochondrial transport along microtubules is mediated by motor proteins, and their movement is influenced by neuronal activity and energy demands. During development, mitochondria support neuronal differentiation and axonogenesis, and their distribution is critical for establishing neuronal polarity. Mitochondrial dysfunction can impair synaptic plasticity, leading to learning and memory deficits. Mitochondria also play a role in synaptic transmission by buffering Ca²+ and providing ATP. In neuronal cell death, mitochondria are involved in both necrosis and apoptosis. Necrosis occurs under severe energy deprivation and oxidative stress, while apoptosis is a programmed process involving mitochondrial permeability transition pores (PTP), cytochrome c release, and caspase activation. Mitochondrial dysfunction can lead to caspase-independent cell death (CIPCD), where AIF is released instead of cytochrome c. Mitochondria are also involved in neurodegenerative diseases, such as Alzheimer's, where amyloid-beta (Aβ) accumulation leads to oxidative stress and Ca²+ dysregulation. Mitochondrial dysfunction in these diseases is associated with impaired energy production, increased ROS, and disrupted Ca²+ homeostasis. Understanding mitochondrial biology and its role in neuronal function and disease is crucial for developing therapeutic strategies to prevent and treat neurological disorders. Advances in mitochondrial research are leading to new approaches for neuroprotection and regeneration.