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[4] Complementary work has reported that Semax and its Pro-Gly-Pro fragment together activate transcription of neurotrophins and their receptor genes after ischemia, reinforcing the picture of a peptide that acts partly by nudging endogenous neurotrophic and inflammatory programs

Elevated iron in the SNpc, reduced glutathione, and widespread oxidation of lipids document the oxidative milieu in post-mortem PD brains, whereas deficits in complex I activity and impaired mitophagy underscore the pivotal role of dysfunctional mitochondria in reactive oxygen species (ROS) overload

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