Alternations in morphometric similarity network in mesial temporal epilepsy correlate to neuroinflammatory pathway

Lu Lu1, Chenyang Zhao1, Weihao Liao1

  • 1Department of Neurology, & Institute of Brain Science and Brain-Inspired Technology, West China Hospital, Sichuan University, Chengdu, 610041, Sichuan, China.

Acta Epileptologica
|April 11, 2025
PubMed
Abstract

Insights

Mesial temporal lobe epilepsy (mTLE) involves brain-wide structural changes linked to neuroinflammation. These alterations, particularly with hippocampal sclerosis, suggest a connection between mTLE and neurodegenerative diseases.

Area of Science:

  • Neuroscience
  • Epileptology
  • Genetics

Background:

  • Mesial temporal lobe epilepsy (mTLE) is the most common focal epilepsy.
  • Hippocampal sclerosis frequently co-occurs with mTLE.
  • Neuroinflammation is increasingly recognized as a key factor in mTLE development and progression.

Purpose of the Study:

  • To investigate structural brain alterations in mTLE using morphometric similarity network (MSN) analysis.
  • To correlate these structural changes with inflammation-related gene expression.
  • To explore the relationship between mTLE, neuroinflammation, and neurodegenerative diseases.

Main Methods:

  • Utilized morphometric similarity network (MSN) analysis.
  • Leveraged the Allen Human Brain Atlas (AHBA) database for structural data.
  • Correlated brain structural changes with inflammation-related gene expression data.

Main Results:

  • Identified widespread structural alterations in frontal and parietal lobes and cingulate cortex.
  • Observed significant correlations between these alterations and neuroinflammatory genes (e.g., PRR5, SMAD3, IRF3).
  • Found a stronger correlation in mTLE patients with hippocampal sclerosis and highlighted pathways linked to neurodevelopment and neurodegeneration.

Conclusions:

  • Brain-wide macroscopic morphometric changes in mTLE correlate with neuroinflammation.
  • Findings provide evidence for a bidirectional link between mTLE and neurodegenerative diseases.
  • Suggests neuroinflammation as a potential therapeutic target in mTLE.

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