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Related Experiment Video

Updated: Jul 4, 2025

Positron Emission Tomography Imaging for In Vivo Measuring of Myelin Content in the Lysolecithin Rat Model of Multiple Sclerosis
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Role of fenofibrate in multiple sclerosis.

Ahmad A Abulaban1,2,3, Hayder M Al-Kuraishy4, Ali I Al-Gareeb4

  • 1College of Medicine, King Saud Bin Abdulaziz University for Health Sciences, Riyadh, Saudi Arabia.

European Journal of Medical Research
|February 9, 2024
PubMed
Summary

Fenofibrate, a PPAR-α agonist, shows potential in treating multiple sclerosis (MS) by reducing neuroinflammation. This review explores how fenofibrate mitigates MS neuropathology through various immune-modulating pathways.

Keywords:
DemyelinationFenofibrateMultiple sclerosisOxidative stress

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Area of Science:

  • Neuroimmunology
  • Pharmacology

Background:

  • Multiple sclerosis (MS) is a primary inflammatory demyelinating disorder of the central nervous system (CNS).
  • MS pathophysiology involves immune-mediated myelin sheath destruction, leading to plaques, inflammation, and neuronal injury.
  • MS plaques are disseminated focal lesions in the CNS white and grey matter.

Purpose of the Study:

  • To review the immunoinflammatory mechanisms by which fenofibrate mitigates multiple sclerosis (MS) neuropathology.
  • To elucidate the role of fenofibrate as a peroxisome proliferator-activated receptor alpha (PPAR-α) agonist in managing MS.

Main Methods:

  • Literature review focusing on the immunomodulatory effects of fenofibrate in MS.
  • Analysis of fenofibrate's impact on inflammatory signaling pathways, including Th17 differentiation.

Main Results:

  • Fenofibrate, a PPAR-α agonist, demonstrates anti-inflammatory properties relevant to MS.
  • Fenofibrate inhibits Th17 cell differentiation by suppressing pro-inflammatory signaling.
  • The drug modulates key pathways implicated in MS, such as oxidative stress and mitochondrial dysfunction.

Conclusions:

  • Fenofibrate can attenuate MS neuropathology.
  • Its therapeutic potential lies in modulating neuroinflammation, oxidative stress, autophagy, mitochondrial dysfunction, and inflammatory signaling pathways.