Inflammation-related microRNA alterations in epilepsy: a systematic review of human and animal studies

Mohammad Javad Yousefi1,2, Ali Rezvanimehr3, Kiarash Saleki4,5

  • 1Student Research Committee, Babol University of Medical Sciences, Babol, 4717647745, Iran.

PubMed

Insights

Inflammation plays a key role in epilepsy. This review highlights how specific microRNAs (miRNAs) are involved in epilepsy

Area of Science:

  • Neurology
  • Molecular Biology
  • Immunology

Background:

  • Epilepsy affects 50 million people globally.
  • Inflammation is increasingly recognized as a key factor in epilepsy development.
  • MicroRNAs (miRNAs) are implicated in epilepsy pathogenesis via regulation of oxidative stress, apoptosis, and inflammation.

Purpose of the Study:

  • To systematically review and summarize the literature on the role of inflammatory microRNAs in epilepsy pathophysiology.
  • To analyze human and animal studies investigating the link between miRNAs and epilepsy.
  • To identify specific miRNAs and their associated signaling pathways in epilepsy.

Main Methods:

  • Systematic review of 21 human and 44 animal studies.
  • Analysis of data on microRNA expression and function in epilepsy.
  • Investigation of common epilepsy induction methods in animal models (Kainic acid, pilocarpine).

Main Results:

  • Upregulated inflammatory miRNAs (e.g., miR-146a, miR-155, miR-132) are associated with epilepsy.
  • Downregulated anti-inflammatory miRNAs (e.g., miR-221, miR-222, miR-29a) show protective effects.
  • MicroRNAs exhibit tissue-specific expression in brain and body fluids, impacting diagnostic and pathophysiological roles.
  • Inflammatory miRNAs modulate key pathways like TLR4/NF-κB, PI3K/Akt, and IL-1β-mediated neuroinflammation.

Conclusions:

  • Inflammatory microRNAs are significantly involved in the pathophysiology of epilepsy.
  • Specific miRNAs show potential as diagnostic biomarkers for epilepsy.
  • Modulating inflammatory miRNAs may offer novel therapeutic targets for epilepsy treatment.