Preclinical (transgenic mouse model) · PMID 41479572
The Potential of Semax and Its Derivative for Correcting Pathological Impairments in Alzheimer's Disease Model — VialBase Research
Semax and derivative improved cognitive function in APPswe/PS1dE9/Blg mice
Last updated · 2025 · Radchenko AI, Kuzubova EV, Apostol AA, et al. · Acta Naturae
Key findings
- Semax and derivative improved cognitive function in APPswe/PS1dE9/Blg mice
- Open field, novel object recognition, and Barnes maze all showed improvement
- Reduced amyloid inclusions in cortex and hippocampus
- Demonstrates high therapeutic potential for AD correction
Semax Reduces Amyloid and Improves Cognition in AD Mice (PMID: 41479572)
Study Design
- APPswe/PS1dE9/Blg transgenic Alzheimer’s mice
- Tested both Semax and a novel derivative
- Behavioral tests: open field, novel object recognition, Barnes maze
- Histological examination of amyloid plaques
Key Results
- Both Semax and its derivative improved cognitive functions across all behavioral tests
- Histology showed reduced amyloid inclusion numbers in cortex and hippocampus
- Derivative may have enhanced potency (details in full paper)
Relevance
Supports Semax as a potential therapeutic for Alzheimer’s disease, addressing both cognitive symptoms and underlying amyloid pathology. The anti-amyloid effect goes beyond symptomatic relief.