The nootropic peptide Semax (ACTH 4-10 analog) increased BDNF and TrkB receptor expression in the rat hippocampus — providing a molecular mechanism for its cognitive-enhancing and neuroprotective effects.
Key findingSemax upregulated BDNF mRNA and TrkB receptor expression in the rat hippocampus, providing the neurotrophic molecular mechanism for its documented cog
What the researchers found
Semax upregulated BDNF mRNA and TrkB receptor expression in the rat hippocampus, providing the neurotrophic molecular mechanism for its documented cognitive enhancement and neuroprotective effects — BDNF is the brain's primary growth and survival factor.
Why it matters
Relevant for semax, neuroprotection, cognitive-enhancement.
How the study worked
animal-study study on semax, neuroprotection.
What this study cannot tell us
See abstract.
How to read the evidence
moderate evidence.
When this study was published
Published in 2006.
The bigger picture
Advances peptide research.
Questions still open
- Further research needed.
- Clinical translation to evaluate.
Common questions
What was studied?
What was found?
Read the original research
Semax, an analog of ACTH(4-10) with cognitive effects, regulates BDNF and trkB expression in the rat hippocampus.
Brain research, 1117(1), 54-60
Citation
Dolotov, Oleg V; Karpenko, Ekaterina A; Inozemtseva, Lyudmila S; Seredenina, Tamara S; Levitskaya, Natalia G; Rozyczka, Joanna; Dubynina, Elena V; Novosadova, Ekaterina V; Andreeva, Lyudmila A; Alfeeva, Lyudmila Yu; Kamensky, Andrey A; Grivennikov, Igor A; Myasoedov, Nikolay F; Engele, Jürgen. (2006). Semax, an analog of ACTH(4-10) with cognitive effects, regulates BDNF and trkB expression in the rat hippocampus.. Brain research, 1117(1), 54-60.