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The myelin sheath acts as an insulating shield, facilitating the rapid propagation of action potentials as well as providing structural and trophic support to neurons (Bradl and Lassmann, 2010)

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Research published in journals including the Journal of Neurochemistry and Brain Research has examined the molecular mechanisms underlying these effects with Semax-induced upregulation of BDNF, NGF, and TrkB identified as key mediators of the observed neuroprotection, alongside modulation of the inflammatory cytokine cascade in peri-infarct brain tissue