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BACKGROUND:The prevalence of neurodegenerative disorders such as Parkinson’s disease (PD) is increased by age.Alleviation of their symptoms and protection of normal neurons against degeneration are the main aspects of the researches to establish novel therapeutic strategies.Many studies have shown that mitochondria as the most important organelles in the brain which show impairment in PD models.Succinate dehydrogenase (SDH) as a component of the oxidative phosphorylation system in mitochondria connects Krebs cycle to the electron transport chain.Dysfunction or inhibition of the SDH can trigger mitochondrial impairment and disruption in ATP generation.Excessive in lipid synthesis and induction of the excitotoxicity as inducers in PD are controlled by SDH activity directly and indirectly.On the other hand,mutation in subunits of the SDH correlates with the onset of neurodegenerative disorders.Therefore,SDH could behave as one of the main regulators in neuroprotection.OBJECTIVE:In this review we will consider contribution of the SDH and its related mechanisms in PD.METHODS:Pubmed search engine was used to find published studies from 1977 to 2016.Succinate dehydrogenase,lipid and brain,mitochondria and Parkinson’s disease were the main keywords for searching in the engine.RESULTS:Wide ranges of studies (59 articles) in neurodegenerative disorders especially Parkinson’s disease like genetics of the Parkinson’s disease,effects of the mutant SDH on cell activity and physiology and lipid alteration in neurodegenerative disorders have been used in this review.CONCLUSION:Mitochondria as key organelles in the energy generation plays crucial roles in PD.ETC complex in this organelle consists four complexes which alteration in their activities cause ROS generation and ATP depletion.Most of complexes are encoded by mtDNA while complex H is the only part of the ETC which is encoded by nuclear genome.So,focusing on the SDH and related pathways which have important role in neuronal survival and SDH has a potential to further studies as a novel neuroprotective agent.