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



Golab F1 ; Hajimirzaei P2 ; Zarbakhsh S3, 4 ; Zolfaghari S5 ; Hayat P1 ; Joghataei MT1 ; Bakhtiarzadeh F6 ; Ahmadirad N1
Authors
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Authors Affiliations
  1. 1. Cellular and Molecular Research Center, Iran University of Medical Sciences, Tehran, Iran
  2. 2. Department of Radiation Sciences, Allied Medicine Faculty, Iranaq, University of Medical Sciences, Tehran, Iran
  3. 3. Nervous System Stem Cells Research Center, Semnan University of Medical Sciences, Semnan, Iran
  4. 4. Department of Anatomy, Faculty of Medicine, Semnan University of Medical Sciences, Semnan, Iran
  5. 5. Department of Tissue Engineering & Regenerative Medicine, Faculty of Advanced Technologies in Medicine, Iran University of Medica Sciences, Tehran, Iran
  6. 6. Department of Neurosurgery, Robert Wood Johnson Medical School, Rutgers University, Piscataway, 08854, NJ, United States

Source: Journal of Molecular Neuroscience Published:2025


Abstract

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. © The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2025.