Emerging Therapeutic Strategies for Epilepsy: Bridging Research and Clinical Practice

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Neurobiology and Clinical Neuroscience".

Deadline for manuscript submissions: 31 October 2025 | Viewed by 1328

Special Issue Editor


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Guest Editor
Department of Molecular and Integrative Physiology, University of Illinois at Urbana-Champaign, Urbana, IL 60801, USA
Interests: epilepsy; status epilepticus; MRI; EEG; inhibitory neurotransmission; immunohistochemistry; gene regulation; neurodegeneration; precision medicine
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Special Issue Information

This Special Issue is focused on advancing novel therapeutic strategies specifically for the treatment of epilepsy, a neurological disorder that remains a significant medical challenge. Epilepsy is characterized by recurrent, unprovoked seizures, and its complex pathophysiology involves genetic, molecular, and environmental factors. Despite advancements in understanding the mechanisms of epilepsy, current treatments often focus on managing symptoms rather than addressing the underlying causes, leaving many patients with limited options and persistent disability.

We invite leading researchers and clinicians to explore breakthroughs in epilepsy treatment, including the development of novel antiseizure medications, gene therapies, and innovative techniques such as neurostimulation. We specially emphasized translational research that bridges the gap between laboratory findings and clinical practice, with the goal of improving outcomes in patients with epilepsy. The issue will highlight emerging therapeutic approaches, such as precision medicine and neuroprotective agents, which offer potential for modifying the course of the disease rather than symptomatic relief.

By addressing key mechanisms such as neuronal hyperexcitability, synaptic dysfunction, and neuroinflammation, this issue seeks to advance our understanding of epileptogenesis and novel treatment strategies. The collection aims to inspire new research directions and foster hope for improved management and care for individuals living with epilepsy.

Dr. Tanveer Singh
Guest Editor

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Keywords

  • epilepsy
  • status epilepticus
  • MRI
  • EEG
  • inhibitory neurotransmission
  • immunohistochemistry
  • gene regulation
  • neurodegeneration
  • precision medicine

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Published Papers (1 paper)

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Research

15 pages, 4094 KiB  
Article
Mossy Fiber Sprouting in Temporal Lobe Epilepsy: The Impact of Netrin-1, DCC, and Gene Expression Changes
by Melis Onay, Patrick N. Harter, Katherina Weber, Albrecht Piiper, Marcus Czabanka, Karl H. Plate, Thomas M. Freiman, Florian Gessler and Barbara Puhahn-Schmeiser
Biomedicines 2024, 12(12), 2869; https://doi.org/10.3390/biomedicines12122869 - 17 Dec 2024
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Abstract
Background: Temporal lobe epilepsy (TLE) is the most common form of drug-resistant epilepsy, often associated with hippocampal sclerosis (HS), which involves selective neuronal loss in the Cornu Ammonis subregion 1 CA1 and CA4 regions of the hippocampus. Granule cells show migration and mossy [...] Read more.
Background: Temporal lobe epilepsy (TLE) is the most common form of drug-resistant epilepsy, often associated with hippocampal sclerosis (HS), which involves selective neuronal loss in the Cornu Ammonis subregion 1 CA1 and CA4 regions of the hippocampus. Granule cells show migration and mossy fiber sprouting, though the mechanisms remain unclear. Microglia play a role in neurogenesis and synaptic modulation, suggesting they may contribute to epilepsy. This study examines the role of microglia and axonal guidance molecules in neuronal reorganization in TLE. Methods: Nineteen hippocampal samples from patients with TLE undergoing epilepsy surgery were analyzed. Microglial activity (M1/M2-like microglia) and neuronal guidance molecules were assessed using microscopy and semi-automated techniques. Gene expression was evaluated using the nCounter Expression Profiling method. Results: Neuronal cell loss was correlated with decreased activity of the M1 microglial phenotype. In the CA2 region, neuronal preservation was linked to increased mossy fiber sprouting and microglial presence. Neuronal markers such as Deleted in Colorectal Cancer (DCC) and Synaptopodin were reduced in areas of cell death, while Netrin-1 was elevated in the granule cell layer, potentially influencing mossy fiber sprouting. The nCounter analysis revealed downregulation of genes involved in neuronal activity (e.g., NPAS4, BCL-2, GRIA1) and upregulation of IκB, indicating reduced neuroinflammation. Conclusions: This study suggests reduced neuroinflammation in areas of neuronal loss, while regions with preserved neurons showed mossy fiber sprouting associated with microglia, Netrin-1, and DCC. Full article
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