Neurological research · 2026
The potential role of metformin in multiple sclerosis: good or bad, and what's the lesson.
СтатьяОбзорНазвание и аннотация: Перевод в очереди
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AlAseeri Ali Abdullah, Al-Kuraishy Hayder M, Al-Gareeb Ali I, Eliwa Duaa, Batiha Gaber El-Saber
Аннотация
OBJECTIVES: To explore and discuss the possible neuroprotective effect of metformin in multiple sclerosis (MS), with emphasis on its metabolic mechanisms, particularly AMP-activated protein kinase (AMPK) activation and growth differentiation factor 15 (GDF15) induction.
METHODS: A narrative review of recent preclinical and clinical studies examining the cellular and molecular effects of metformin relevant to neurodegeneration and MS was conducted. Literature addressing mitochondrial function, inflammatory signaling, oxidative stress, and metabolic pathways modulated by metformin were analyzed to elucidate its potential mechanisms in MS.
RESULTS: Findings across multiple studies indicate that metformin exerts neuroprotective effects by modulating mitochondrial homeostasis, reducing oxidative stress, and attenuating pro-inflammatory pathways. Metformin has been shown to influence immune-inflammatory responses, improve metabolic balance in neural and immune cells, and potentially ameliorate pathological processes associated with disease progression in both human MS and animal models.
DISCUSSION: Metformin demonstrates promising potential as an adjunct therapeutic agent in MS due to its capacity to modulate key metabolic and inflammatory pathways involved in neurodegeneration and neuroinflammation. Although current evidence supports its beneficial effects, the precise mechanisms by which metformin influences MS pathophysiology remain partially elucidated. Further targeted studies are required to clarify these mechanisms and to determine its clinical relevance in neuroimmune modulation and MS management.
METHODS: A narrative review of recent preclinical and clinical studies examining the cellular and molecular effects of metformin relevant to neurodegeneration and MS was conducted. Literature addressing mitochondrial function, inflammatory signaling, oxidative stress, and metabolic pathways modulated by metformin were analyzed to elucidate its potential mechanisms in MS.
RESULTS: Findings across multiple studies indicate that metformin exerts neuroprotective effects by modulating mitochondrial homeostasis, reducing oxidative stress, and attenuating pro-inflammatory pathways. Metformin has been shown to influence immune-inflammatory responses, improve metabolic balance in neural and immune cells, and potentially ameliorate pathological processes associated with disease progression in both human MS and animal models.
DISCUSSION: Metformin demonstrates promising potential as an adjunct therapeutic agent in MS due to its capacity to modulate key metabolic and inflammatory pathways involved in neurodegeneration and neuroinflammation. Although current evidence supports its beneficial effects, the precise mechanisms by which metformin influences MS pathophysiology remain partially elucidated. Further targeted studies are required to clarify these mechanisms and to determine its clinical relevance in neuroimmune modulation and MS management.