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Yamashita H, Matsuhara H, Miotani S, Sako Y, Matsui T, Tanaka H, Inagaki N

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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

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In vitro anti-oxidation, anti-inflammation, anti-bacteria, and cell homing Inflammation and oxidative stress are two main pathological signs of progression in OA 39

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