Scholarlink

<p>Epilepsy is a common neurological disorder that is increasingly recognized for its significant association with mitochondrial dysfunction. This review explores the intricate relationship between mitochondrial dysfunction and epilepsy, highlighting the molecular mechanisms, diagnostic strategies, and therapeutic approaches involved. Mitochondrial abnormalities, including defects in the electron transport chain, impaired mitochondrial dynamics, disrupted autophagy, and increased oxidative stress, are implicated in epilepsy pathogenesis. The molecular mechanisms involve respiratory chain impairments, fission–fusion imbalances, inadequate mitophagy, and oxidative stress-induced neuronal excitability. The diagnosis of mitochondrial epilepsy requires a multifaceted approach, combining clinical assessment, biochemical testing, imaging, and genetic analysis, with a particular focus on mtDNA mutations. Therapeutic strategies include antiepileptic drugs with variable mitochondrial effects, the ketogenic diet, and emerging potential approaches such as antioxidants and mitochondrial-targeted therapies. Despite advances in understanding and treatment, challenges persist due to the complexity of mtDNA mutations and treatment resistance. Future directions involve gene-editing technologies, mitochondrial transplantation, and induced pluripotent stem cells, which hold promise for addressing the underlying defects and improving epilepsy management.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Mitochondrial dysfunction in epilepsy: mechanistic insights and clinical strategies

  • 期刊论文

  • 发表日期：

    2025年5月20日

查看全文
  • Xiaolu Zhang,
  • Zhengjuan Wu,
  • Xu Zhou,
  • Hua Tao

摘要

Epilepsy is a common neurological disorder that is increasingly recognized for its significant association with mitochondrial dysfunction. This review explores the intricate relationship between mitochondrial dysfunction and epilepsy, highlighting the molecular mechanisms, diagnostic strategies, and therapeutic approaches involved. Mitochondrial abnormalities, including defects in the electron transport chain, impaired mitochondrial dynamics, disrupted autophagy, and increased oxidative stress, are implicated in epilepsy pathogenesis. The molecular mechanisms involve respiratory chain impairments, fission–fusion imbalances, inadequate mitophagy, and oxidative stress-induced neuronal excitability. The diagnosis of mitochondrial epilepsy requires a multifaceted approach, combining clinical assessment, biochemical testing, imaging, and genetic analysis, with a particular focus on mtDNA mutations. Therapeutic strategies include antiepileptic drugs with variable mitochondrial effects, the ketogenic diet, and emerging potential approaches such as antioxidants and mitochondrial-targeted therapies. Despite advances in understanding and treatment, challenges persist due to the complexity of mtDNA mutations and treatment resistance. Future directions involve gene-editing technologies, mitochondrial transplantation, and induced pluripotent stem cells, which hold promise for addressing the underlying defects and improving epilepsy management.