AI Article Synopsis
- Scientists developed a new juvenile murine model to study social interaction deficits in demyelinating diseases, highlighting the impact of such conditions on social behavior.
- Metformin, an FDA-approved medication, was found to promote the regeneration of oligodendrocytes and improve social interactions in this model by activating specific molecular pathways.
- Specifically, metformin enhances oligodendrocyte precursor cell (OPC) growth and maturation, suggesting it could be a promising treatment for addressing social interaction issues related to juvenile demyelination.
Article Abstract
Individuals with demyelinating diseases often experience difficulties during social interactions that are not well studied in preclinical models. Here, we describe a novel juvenile focal corpus callosum demyelination murine model exhibiting a social interaction deficit. Using this preclinical murine demyelination model, we discover that application of metformin, an FDA-approved drug, in this model promotes oligodendrocyte regeneration and remyelination and improves the social interaction. This beneficial effect of metformin acts through stimulating Ser436 phosphorylation in CBP, a histone acetyltransferase. In addition, we found that metformin acts through two distinct molecular pathways to enhance oligodendrocyte precursor (OPC) proliferation and differentiation, respectively. Metformin enhances OPC proliferation through early-stage autophagy inhibition, while metformin promotes OPC differentiation into mature oligodendrocytes through activating CBP Ser436 phosphorylation. In summary, we identify that metformin is a promising remyelinating agent to improve juvenile demyelination-associated social interaction deficits by promoting oligodendrocyte regeneration and remyelination.
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| http://dx.doi.org/10.1016/j.expneurol.2020.113454 | DOI Listing |
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