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The mechanistic work behind that reasoning is preclinical: in Wistar rats given intranasal Semax, the peptide increased BDNF expression and TrkB phosphorylation in the hippocampus, which shows a neurotrophic mechanism in an animal model and does not establish cognitive efficacy or the safety of subcutaneous regimens in humans (Dolotov and colleagues, Brain Research 2006, on how Semax regulates BDNF and trkB expression in the rat hippocampus
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