Low field magnetic stimulation promotes myelin repair and cognitive recovery in chronic cuprizone mouse model

Background Multiple sclerosis (MS) is an inflammatory demyelinating disease featured with neuroinflammation, demyelination, and the loss of oligodendrocytes. Cognitive impairment and depression are common neuropsychiatric symptoms in MS that are poorly managed with the present interventions. Objective This study aimed to investigate the effects of low field magnetic stimulation (LFMS), a novel non‐invasive neuromodulation technology, on cognitive impairment and depressive symptoms associated with MS using a mouse model of demyelination. Methods C57BL female mice were fed with a 0.2% cuprizone diet for 12 weeks to induce a chronic demyelinating model followed by 4 weeks of cuprizone withdrawal with either sham or LFMS treatment. Results Improved cognition and depression‐like behaviour and restored weight gain were observed in mice with LFMS treatment. Immunohistochemical and immunoblotting data showed enhanced myelin basic protein (MBP) and myelin oligodendrocyte glycoprotein expressions (MOG) in the prefrontal cortex of mice with LFMS treatment, supporting that myelin repair was promoted. LFMS also increased the protein expression of mature oligodendrocyte biomarker glutathione‐S‐transferase (GST‐π). In addition, expression of TGF‐β and associated receptors were elevated with LFMS treatment, implicating this pathway in the response. Conclusion Results from the present study revealed LFMS to have neuroprotective effects, suggesting that LFMS has potential therapeutic value for treating cognitive impairment and depression related to demyelination disorders. Low field magnetic stimulation (LFMS) is a non‐invasive brain stimulation device that improved cognition and depression‐like behaviour and promoted myelin repair and oligodendrocyte maturation in a chronic cuprizone intoxication animal model. The transforming growth factor‐beta signaling pathway may be activated due to LFMS. This study suggests that LFMS has therapeutic potential in demyelinating diseases and related cognitive impairment and depression.