Superoxide dismutase (SOD) is a key antioxidant enzyme that detoxifies reactive oxygen species (ROS) and maintains redox balance in cells. SODs are found in neurons and glial cells throughout the central nervous system (CNS), both intracellularly and extracellularly. SODs play a crucial role in preventing oxidative stress (OS), which is linked to various neurological disorders, including neurodegenerative diseases like Alzheimer's, Parkinson's, Huntington's, and Down syndrome. SODs convert superoxide radicals into less harmful molecules, such as hydrogen peroxide and oxygen, and are essential for protecting neurons from oxidative damage. SODs also act as anti-inflammatory agents and may serve as potential therapeutic targets for neurological disorders. SODs are classified into three main types based on their metal cofactors: Cu/Zn-SOD (SOD1), Mn-SOD (SOD2), and extracellular Cu/Zn-SOD (SOD3). SOD1 is primarily found in the cytosol, SOD2 in mitochondria, and SOD3 in extracellular tissues. SODs are involved in various physiological processes, including redox regulation, neuroprotection, and modulation of inflammatory responses. SOD mimetics, such as Metalloporphyrin Mn(II)-cyclic polyamines, Nitroxides, and Mn(III)-Salen complexes, are used therapeutically in neurological disorders due to their ability to mimic SOD activity. SODs are implicated in the pathogenesis of several neurological disorders. In Alzheimer's disease, SOD activity is reduced, and SOD deficiency is associated with increased amyloid-beta plaques and oxidative damage. In Parkinson's disease, SOD deficiency leads to increased ROS production and neuronal death. In Huntington's disease, mutant huntingtin protein disrupts mitochondrial function and increases ROS, leading to neuronal loss. In Down syndrome, the trisomy of chromosome 21 leads to increased SOD1 expression and OS, contributing to neurological symptoms. SODs also play a role in ischemic stroke by reducing oxidative damage and neuroinflammation. SOD mimetics have shown promise in treating stroke by improving neurological outcomes and reducing infarct size. In depression and schizophrenia, SOD activity is altered, with increased OS levels and reduced antioxidant defenses. SOD levels are associated with symptom severity in these disorders. Overall, SODs are essential for maintaining redox balance and protecting the CNS from oxidative damage. SOD mimetics and SOD-based therapies are promising approaches for treating neurological disorders by reducing oxidative stress and neuroinflammation.Superoxide dismutase (SOD) is a key antioxidant enzyme that detoxifies reactive oxygen species (ROS) and maintains redox balance in cells. SODs are found in neurons and glial cells throughout the central nervous system (CNS), both intracellularly and extracellularly. SODs play a crucial role in preventing oxidative stress (OS), which is linked to various neurological disorders, including neurodegenerative diseases like Alzheimer's, Parkinson's, Huntington's, and Down syndrome. SODs convert superoxide radicals into less harmful molecules, such as hydrogen peroxide and oxygen, and are essential for protecting neurons from oxidative damage. SODs also act as anti-inflammatory agents and may serve as potential therapeutic targets for neurological disorders. SODs are classified into three main types based on their metal cofactors: Cu/Zn-SOD (SOD1), Mn-SOD (SOD2), and extracellular Cu/Zn-SOD (SOD3). SOD1 is primarily found in the cytosol, SOD2 in mitochondria, and SOD3 in extracellular tissues. SODs are involved in various physiological processes, including redox regulation, neuroprotection, and modulation of inflammatory responses. SOD mimetics, such as Metalloporphyrin Mn(II)-cyclic polyamines, Nitroxides, and Mn(III)-Salen complexes, are used therapeutically in neurological disorders due to their ability to mimic SOD activity. SODs are implicated in the pathogenesis of several neurological disorders. In Alzheimer's disease, SOD activity is reduced, and SOD deficiency is associated with increased amyloid-beta plaques and oxidative damage. In Parkinson's disease, SOD deficiency leads to increased ROS production and neuronal death. In Huntington's disease, mutant huntingtin protein disrupts mitochondrial function and increases ROS, leading to neuronal loss. In Down syndrome, the trisomy of chromosome 21 leads to increased SOD1 expression and OS, contributing to neurological symptoms. SODs also play a role in ischemic stroke by reducing oxidative damage and neuroinflammation. SOD mimetics have shown promise in treating stroke by improving neurological outcomes and reducing infarct size. In depression and schizophrenia, SOD activity is altered, with increased OS levels and reduced antioxidant defenses. SOD levels are associated with symptom severity in these disorders. Overall, SODs are essential for maintaining redox balance and protecting the CNS from oxidative damage. SOD mimetics and SOD-based therapies are promising approaches for treating neurological disorders by reducing oxidative stress and neuroinflammation.