The onset of neurodegenerative diseases like Alzheimer’s, Parkinson’s, and Huntington’s increases with age. Research focuses on finding new therapies to alleviate symptoms and protect neurons from degeneration. Mitochondria play a crucial role in high-energy tissues such as the brain. Impairments in mitochondrial function can render neurons vulnerable to stress and death. Succinate dehydrogenase (SDH) links the tricarboxylic acid (TCA) cycle and electron transport chain. Dysfunctional SDH could therefore impair mitochondrial activity, adenosine triphosphate (ATP) production, and neuronal energy homeostasis. Furthermore, SDH may control excess lipid synthesis and excitotoxicity in neurodegeneration through direct and indirect means. SDH mutations are also associated with these diseases’ onset. Given its central metabolic role, SDH could act as a key regulator of neuroprotection. This chapter presents recent findings on SDH activity and related pathways that may promote neuronal survival. We also discuss the neuroprotective potential of SDH. Elucidating the precise mechanisms of SDH could uncover new therapeutic targets for neurodegenerative disorders.

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Neurodegenerative Diseases and Succinate Dehydrogenase: A Therapeutics Avenue for Treatment

  • Viswapriya Viswalingam,
  • Dileep Kumar

摘要

The onset of neurodegenerative diseases like Alzheimer’s, Parkinson’s, and Huntington’s increases with age. Research focuses on finding new therapies to alleviate symptoms and protect neurons from degeneration. Mitochondria play a crucial role in high-energy tissues such as the brain. Impairments in mitochondrial function can render neurons vulnerable to stress and death. Succinate dehydrogenase (SDH) links the tricarboxylic acid (TCA) cycle and electron transport chain. Dysfunctional SDH could therefore impair mitochondrial activity, adenosine triphosphate (ATP) production, and neuronal energy homeostasis. Furthermore, SDH may control excess lipid synthesis and excitotoxicity in neurodegeneration through direct and indirect means. SDH mutations are also associated with these diseases’ onset. Given its central metabolic role, SDH could act as a key regulator of neuroprotection. This chapter presents recent findings on SDH activity and related pathways that may promote neuronal survival. We also discuss the neuroprotective potential of SDH. Elucidating the precise mechanisms of SDH could uncover new therapeutic targets for neurodegenerative disorders.