Amelioration of Alzheimer's-Type Pathological Impairments with Semax

Journal Context: Acta Naturae / Europe PMC (Published Late 2025) | Identifiers: Article PMC12755871

Principal Investigators: Scientific Registry Core (Belgorod State University Research Institute of Pharmacology)

Methodology: Evaluation of transgenic $\text{APPswe/PS1dE9/Blg}$ male mice, which serve as an aggressive mammalian model for Alzheimer's disease. The experimental cohorts were administered regular cycles of Semax to track behavioral changes across open field, novel object recognition, and Barnes maze tests, followed by detailed histological staging of cerebral cortex tissue.

Key Findings: Semax therapy successfully rescued cognitive performance metrics across all behavioral testing environments, restoring memory retention and target-seeking focus in the Barnes maze. Histological examinations of the brain tissue confirmed the underlying structural cause: Semax administration significantly reduced the total number of neurotoxic amyloid inclusions (plaques) within both the cortex and the hippocampus. This reduction was further supported by independent data showing that Semax reduces destructive reactive oxygen species (ROS) caused by amyloid-copper toxicity, confirming its dual status as an operational nootropic and a physical shield against degenerative tissue erosion.