ArticleThe American journal of pathology2013
AMP-activated protein kinase signaling protects oligodendrocytes that restore central nervous system functions in an experimental autoimmune encephalomyelitis model.
Article in The American journal of pathology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 57 citations in OpenAlex.
- The impact of metformin use on the outcomes of relapse-remitting multiple sclerosis patients receiving interferon beta 1a: an exploratory prospective phase II open-label randomized controlled trial.Journal of neurology · 2024Trial
- Adjunctive Non-Disease-Modifying Therapies in Multiple Sclerosis: Immunometabolic, Neuroprotective and Remyelination-Oriented Approaches.International journal of molecular sciences · 2026Review
- Role of Folate Metabolism in Neurodegenerative Diseases: Insight from Experimental and Clinical Studies.Current nutrition reports · 2026Review
- 2'-deoxyinosine ameliorates multiple sclerosis through modulating Th1/Th2 and Th17/Treg cell balance with potential involvement of AMPK phosphorylation.Frontiers in pharmacology · 2026Article
- Review
- The Possible Role of Metformin and Fibroblast Growth Factor-21 in Multiple Sclerosis Neuropathology: Birds of a Feather Flock Together.The European journal of neuroscience · 2025Review
- Randomized, double-blind, placebo-controlled pilot study of metformin as an adjunctive therapy in Parkinson's disease.Frontiers in pharmacology · 2025Article
- Neuroprotective effect of curcumin against experimental autoimmune encephalomyelitis-induced cognitive and physical impairments in mice: an insight into the role of the AMPK/SIRT1 pathway.Inflammopharmacology · 2024Article
- A metformin add-on clinical study in multiple sclerosis to evaluate brain remyelination and neurodegeneration (MACSiMiSE-BRAIN): study protocol for a multi-center randomized placebo controlled clinical trial.Frontiers in immunology · 2024Article
- The Roles of Caloric Restriction Mimetics in Central Nervous System Demyelination and Remyelination.Current issues in molecular biology · 2023Review
- Metformin attenuates white matter injury and cognitive impairment induced by chronic cerebral hypoperfusion.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2023Article
- The development and benefits of metformin in various diseases.Frontiers of medicine · 2023Review
- Metformin: A Review of Potential Mechanism and Therapeutic Utility Beyond Diabetes.Drug design, development and therapy · 2023Review
- The AMPK activator metformin improves recovery from demyelination by shifting oligodendrocyte bioenergetics and accelerating OPC differentiation.Frontiers in cellular neuroscience · 2023Article
- Metformin Therapy Attenuates Pro-inflammatory Microglia by Inhibiting NF-κB in Cuprizone Demyelinating Mouse Model of Multiple Sclerosis.Neurotoxicity research · 2021Article
- Metformin treatment confers protection of the optic nerve following photoreceptor degeneration.Anatomy & cell biology · 2021Article
- Repurposing metformin to treat age-related neurodegenerative disorders and ischemic stroke.Life sciences · 2021Review
- Beneficial Effects of Metformin on the Central Nervous System, with a Focus on Epilepsy and Lafora Disease.International journal of molecular sciences · 2021Review
- Metformin activated AMPK signaling contributes to the alleviation of LPS-induced inflammatory responses in bovine mammary epithelial cells.BMC veterinary research · 2021Article
- Metformin as a potential therapeutic for neurological disease: mobilizing AMPK to repair the nervous system.Expert review of neurotherapeutics · 2021Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
AMP-activated protein kinase (AMPK) signaling is reported to protect neurons under pathologic conditions; however, its effect on oligodendrocytes (OLs) remains to be elucidated. We investigated whether AMPK signaling protects OLs to restore central nervous system (CNS) functions in an experimental autoimmune encephalomyelitis (EAE), a murine model of multiple sclerosis. Increased inflammation and demyelination in the CNS and peripheral immune responses were consistent with the observed clinical impairments in EAE animals, which were attenuated by treatment with metformin compared with vehicle. In addition, expressions of neurotrophic factors and of signatory genes of OL lineages were increased in the CNS of metformin-treated EAE animals. Likewise, metformin attenuated inflammatory response and enhanced expressions of neurotrophic factors, thereby protecting OLs via AMPK activation in mixed glial cultures stimulated with lipopolysaccharide/interferon γ in vitro, as evidenced by analysis of the expression of signatory genes of O1(+)/MBP(+) OLs and their cellular populations. Metformin also attenuated oxidative stress and malondialdehyde-containing protein levels, with corresponding induction of antioxidative defenses in OLs exposed to cytokines via AMPK activation. These effects of metformin were evident in the CNS of EAE animals. These data provide evidence that AMPK signaling is crucial to protect OLs and, thus, CNS functions in EAE animals. We conclude that AMPK activators, including metformin, have the potential to limit neurologic deficits in multiple sclerosis and related neurodegenerative disorders.
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