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Updated: Jul 4, 2025

Positron Emission Tomography Imaging for In Vivo Measuring of Myelin Content in the Lysolecithin Rat Model of Multiple Sclerosis
Published on: February 28, 2021
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.
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.
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.
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