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Background <p>Mesial temporal lobe epilepsy (mTLE) is the most common form of focal epilepsy, often associated with hippocampal sclerosis. Increasing evidence suggests the pivotal role of neuroinflammation in mTLE onset and progression.</p> Methods <p>We used morphometric similarity network (MSN) analysis and the Allen Human Brain Atlas (AHBA) database to investigate structural changes between mTLE and healthy controls, as well as correlation with inflammation-related gene expression.</p> Results <p>We identified widespread alterations across the frontal and parietal lobes and cingulate cortex linked to neuroinflammatory genes such as <i>PRR5, SMAD3</i>, and <i>IRF3</i>. This correlation was even more pronounced in mTLE patients&#xa0;with hippocampal sclerosis&#xa0;compared to those without. Enrichment analysis highlighted pathways related to neurodevelopment and neurodegeneration, supporting a bidirectional link between mTLE and neurodegenerative diseases.</p> Conclusions <p>These findings suggest that brain-wide macroscopic morphometric alternations in mTLE are correlated to the neuroinflammation process. It provides circumstantial evidence from a new perspective to support the bidirectional link between mTLE and neurodegenerative diseases.</p>

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

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年3月4日

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  • Lu Lu,
  • Chenyang Zhao,
  • Weihao Liao,
  • Peiyu Wang,
  • Yingying Zhang,
  • Dongmei An,
  • Xintong Wu,
  • Hesheng Zhang,
  • Ping Jiang,
  • Yaohui He,
  • Jinpeng Niu,
  • Wei Li,
  • Kangjia Chen,
  • Su Lui,
  • Yu Zhao,
  • Qiyong Gong,
  • Bo Wang,
  • Wei Liao,
  • Josemir W. Sander,
  • Lin Chen,
  • Dong Zhou

摘要

Background

Mesial temporal lobe epilepsy (mTLE) is the most common form of focal epilepsy, often associated with hippocampal sclerosis. Increasing evidence suggests the pivotal role of neuroinflammation in mTLE onset and progression.

Methods

We used morphometric similarity network (MSN) analysis and the Allen Human Brain Atlas (AHBA) database to investigate structural changes between mTLE and healthy controls, as well as correlation with inflammation-related gene expression.

Results

We identified widespread alterations across the frontal and parietal lobes and cingulate cortex linked to neuroinflammatory genes such as PRR5, SMAD3, and IRF3. This correlation was even more pronounced in mTLE patients with hippocampal sclerosis compared to those without. Enrichment analysis highlighted pathways related to neurodevelopment and neurodegeneration, supporting a bidirectional link between mTLE and neurodegenerative diseases.

Conclusions

These findings suggest that brain-wide macroscopic morphometric alternations in mTLE are correlated to the neuroinflammation process. It provides circumstantial evidence from a new perspective to support the bidirectional link between mTLE and neurodegenerative diseases.