article · European journal of medical research
Multiple sclerosis is the most common inflammatory and demyelinating condition affecting the central nervous system, driven by immune-mediated damage to the protective myelin sheath surrounding nerve fibres. This neurodegenerative process leads to the formation of demyelinating plaques, widespread inflammation, and structural nerve injury across the brain and spinal cord. Fenofibrate, an activator of peroxisome proliferator-activated receptor alpha, displays therapeutic potential by dampening harmful immune responses linked to the disease. It suppresses the differentiation of inflammatory Th17 cells through the inhibition of pro-inflammatory signalling pathways. Furthermore, fenofibrate counteracts multiple sclerosis neuropathology through diverse cellular mechanisms, including the reduction of neuroinflammation and oxidative stress, regulation of autophagy, and improvement of mitochondrial dysfunction. These combined actions highlight a broad immunomodulatory and protective profile against the destructive cellular drivers of the disease.
Multiple sclerosis causes progressive nerve damage by stripping away the protective covering of neurons, creating a pressing need for effective protective treatments. By targeting several biological processes simultaneously, including cellular energy deficits, oxidative stress, and chronic inflammation, fenofibrate points towards mechanisms that could help shield the central nervous system from ongoing immune-mediated injury.
This mechanistic review highlights fenofibrate as a potential candidate for drug repurposing or therapeutic development aimed at multiple sclerosis. Pharmaceutical companies and neurodegenerative drug developers are the primary potential users of these insights. Because the evidence is limited to review-level mechanistic findings, the research is at an early conceptual stage and remains distant from clinical use, requiring extensive preclinical validation and dedicated clinical trials.
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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.
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DOI: 10.1186/s40001-024-01700-2
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