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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.
Abstract:
Multiple sclerosis (MS) is the most frequent inflammatory and demyelinating disease of the central nervous system (CNS). The underlying pathophysiology of MS is the destruction of myelin sheath by immune cells. The formation of myelin plaques, inflammation, and injury of neuronal myelin sheath characterizes its neuropathology. MS plaques are multiple focal regions of demyelination disseminated in the brain's white matter, spinal cords, deep grey matter, and cerebral cortex. Fenofibrate is a peroxisome proliferative activated receptor alpha (PPAR-α) that attenuates the inflammatory reactions in MS. Fenofibrate inhibits differentiation of Th17 by inhibiting the expression of pro-inflammatory signaling. According to these findings, this review intended to illuminate the mechanistic immunoinflammatory role of fenofibrate in mitigating MS neuropathology. In conclusion, fenofibrate can attenuate MS neuropathology by modulating different pathways, including oxidative stress, autophagy, mitochondrial dysfunction, inflammatory-signaling pathways, and neuroinflammation.
Insights
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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