Neurodegenerative diseases including Alzheimer’s, Parkinson’s, and Huntington’s disease are becoming more prevalent as people age. Reducing clinical symptoms and shielding neurons from degradation are the primary goals of studies to develop novel treatment approaches. Numerous studies have shown that mitochondria are essential to high-energy tissues like the brain. A disturbance in the physiology or function of the mitochondria may expose neurons to stress and deterioration. Succinate dehydrogenase (SDH) is the enzyme that joins the electron transport chain and the tricarboxylic cycle. As a result, SDH failure may affect the cell’s ability to produce ATP, maintain energy homeostasis, and function of the mitochondria. Beyond the production of lipids, SDH may regulate the generation of excitotoxicity in neurodegenerative diseases via direct and indirect mechanisms. Furthermore, there is a correlation between the start of neurodegenerative diseases and mutation in SDH. SDH may therefore act as a crucial regulator in neuroprotection. This review will include current research on SDH activity and associated pathways that may be crucial for neuronal survival. We will also talk about every potential SDH candidate as a neuroprotective agent.