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The Possible Role of Metformin and Fibroblast Growth Factor‐21 in Multiple Sclerosis Neuropathology: Birds of a Feather Flock Together.

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Title: The Possible Role of Metformin and Fibroblast Growth Factor‐21 in Multiple Sclerosis Neuropathology: Birds of a Feather Flock Together.
Authors: Abulaban, Ahmad A. (AUTHOR), Al‐kuraishy, Hayder M. (AUTHOR), Al‐Gareeb, Ali I. (AUTHOR), Ahmed, Eman A. (AUTHOR), Alruwaili, Mubarak (AUTHOR), Alexiou, Athanasios (AUTHOR), Papadakis, Marios (AUTHOR), El‐Saber Batiha, Gaber (AUTHOR)
Source: European Journal of Neuroscience. Apr2025, Vol. 61 Issue 7, p1-18. 18p.
Subjects: Multiple sclerosis, Metformin, Fibroblast growth factors, Demyelination, Neuroprotective agents, Oxidative stress, Neurological disorders, Myelination
Abstract: Multiple sclerosis (MS) is a progressive demyelinating disease of the CNS, characterized by inflammation, the formation of CNS plaques, and damage to the neuronal myelin sheath (Graphical abstract). Fibroblast growth factor 21 (FGF21) is involved in various metabolic disorders and neurodegenerative diseases. FGF21 and its co‐receptor β‐Kloth are essential in the remyelination process of MS. Metformin, an insulin‐sensitizing drug that is the first‐line treatment for type 2 diabetes mellitus (T2DM), may have a potential neuroprotective impact by up‐regulating the production of FGF21, which may prevent the onset of neurodegenerative diseases including MS. The purpose of this review is to clarify how metformin affects MS neuropathology mechanistically via modifying FGF21. Metformin increases the expression of FGF21. Metformin also increases the expression of β‐Klotho, modulates oxidative stress, reduces glutamate‐induced excitotoxicity, and regulates platelet function and coagulation cascades. In conclusion, metformin can enhance the functional activity of FGF21 in counteracting the development and progression of MS. Preclinical and clinical studies are warranted in this regard. [ABSTRACT FROM AUTHOR]
Copyright of European Journal of Neuroscience is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
Database: Psychology and Behavioral Sciences Collection
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  Data: The Possible Role of Metformin and Fibroblast Growth Factor‐21 in Multiple Sclerosis Neuropathology: Birds of a Feather Flock Together.
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  Data: <searchLink fieldCode="AR" term="%22Abulaban%2C+Ahmad A%2E%22">Abulaban, Ahmad A.</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Al‐kuraishy%2C+Hayder M%2E%22">Al‐kuraishy, Hayder M.</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Al‐Gareeb%2C+Ali I%2E%22">Al‐Gareeb, Ali I.</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Ahmed%2C+Eman A%2E%22">Ahmed, Eman A.</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Alruwaili%2C+Mubarak%22">Alruwaili, Mubarak</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Alexiou%2C+Athanasios%22">Alexiou, Athanasios</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Papadakis%2C+Marios%22">Papadakis, Marios</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22El‐Saber Batiha%2C+Gaber%22">El‐Saber Batiha, Gaber</searchLink> (AUTHOR)
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  Data: <searchLink fieldCode="JN" term="%22European+Journal+of+Neuroscience%22">European Journal of Neuroscience</searchLink>. Apr2025, Vol. 61 Issue 7, p1-18. 18p.
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  Data: <searchLink fieldCode="DE" term="%22Multiple+sclerosis%22">Multiple sclerosis</searchLink><br /><searchLink fieldCode="DE" term="%22Metformin%22">Metformin</searchLink><br /><searchLink fieldCode="DE" term="%22Fibroblast+growth+factors%22">Fibroblast growth factors</searchLink><br /><searchLink fieldCode="DE" term="%22Demyelination%22">Demyelination</searchLink><br /><searchLink fieldCode="DE" term="%22Neuroprotective+agents%22">Neuroprotective agents</searchLink><br /><searchLink fieldCode="DE" term="%22Oxidative+stress%22">Oxidative stress</searchLink><br /><searchLink fieldCode="DE" term="%22Neurological+disorders%22">Neurological disorders</searchLink><br /><searchLink fieldCode="DE" term="%22Myelination%22">Myelination</searchLink>
– Name: Abstract
  Label: Abstract
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  Data: Multiple sclerosis (MS) is a progressive demyelinating disease of the CNS, characterized by inflammation, the formation of CNS plaques, and damage to the neuronal myelin sheath (Graphical abstract). Fibroblast growth factor 21 (FGF21) is involved in various metabolic disorders and neurodegenerative diseases. FGF21 and its co‐receptor β‐Kloth are essential in the remyelination process of MS. Metformin, an insulin‐sensitizing drug that is the first‐line treatment for type 2 diabetes mellitus (T2DM), may have a potential neuroprotective impact by up‐regulating the production of FGF21, which may prevent the onset of neurodegenerative diseases including MS. The purpose of this review is to clarify how metformin affects MS neuropathology mechanistically via modifying FGF21. Metformin increases the expression of FGF21. Metformin also increases the expression of β‐Klotho, modulates oxidative stress, reduces glutamate‐induced excitotoxicity, and regulates platelet function and coagulation cascades. In conclusion, metformin can enhance the functional activity of FGF21 in counteracting the development and progression of MS. Preclinical and clinical studies are warranted in this regard. [ABSTRACT FROM AUTHOR]
– Name: AbstractSuppliedCopyright
  Label:
  Group: Ab
  Data: <i>Copyright of European Journal of Neuroscience is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.)
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        Value: 10.1111/ejn.70067
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        Text: English
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      – SubjectFull: Metformin
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      – SubjectFull: Fibroblast growth factors
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      – SubjectFull: Demyelination
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      – SubjectFull: Neuroprotective agents
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      – SubjectFull: Oxidative stress
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      – SubjectFull: Neurological disorders
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      – SubjectFull: Myelination
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              Text: Apr2025
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