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<p>Glioblastoma multiforme (GBM) is the most aggressive form of primary brain cancer in adults and is characterized by poor prognosis and a high incidence of seizures due to tumor-induced alterations in cerebral physiology. This review explores the complex interactions between GBM-induced neuroinflammation and epilepsy, emphasizing the mechanisms of epileptogenesis influenced by blood–brain barrier dysfunction, ion homeostasis, and neurotransmitter dynamics. We discuss the roles of pro-inflammatory mediators such as interleukin-1β and tumor necrosis factor-alpha in exacerbating excitatory synaptic activity while inhibiting inhibitory signaling, thus creating a milieu conducive to seizure activity. Furthermore, we evaluated the efficacy of current anti-seizure medications and emerging therapeutic strategies, including the reprogramming of tumor-associated macrophages, in managing GBM-related epilepsy and tumor growth. This study aimed to elucidate the critical pathways connecting GBM and epilepsy, thereby advancing our understanding of potential interventional approaches to improve patient outcomes.</p>

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Interplay of Neuroinflammation and Epilepsy in Glioblastoma Multiforme: Mechanisms and Therapeutic Implications

  • 期刊论文

  • 发表日期：

    2025年5月20日

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  • Fereshteh Golab,
  • Pooya Hajimirzaei,
  • Sam Zarbakhsh,
  • Samira Zolfaghari,
  • Parisa Hayat,
  • Mohammad Taghi Joghataei,
  • Fatemeh Bakhtiarzadeh,
  • Nooshin Ahmadirad

摘要

Glioblastoma multiforme (GBM) is the most aggressive form of primary brain cancer in adults and is characterized by poor prognosis and a high incidence of seizures due to tumor-induced alterations in cerebral physiology. This review explores the complex interactions between GBM-induced neuroinflammation and epilepsy, emphasizing the mechanisms of epileptogenesis influenced by blood–brain barrier dysfunction, ion homeostasis, and neurotransmitter dynamics. We discuss the roles of pro-inflammatory mediators such as interleukin-1β and tumor necrosis factor-alpha in exacerbating excitatory synaptic activity while inhibiting inhibitory signaling, thus creating a milieu conducive to seizure activity. Furthermore, we evaluated the efficacy of current anti-seizure medications and emerging therapeutic strategies, including the reprogramming of tumor-associated macrophages, in managing GBM-related epilepsy and tumor growth. This study aimed to elucidate the critical pathways connecting GBM and epilepsy, thereby advancing our understanding of potential interventional approaches to improve patient outcomes.