Researchers have widely discussed the neurogenic and neurorestorative potential of the synthetic peptide N-Acetyl Semax. Research suggests that memory and cognitive function may be enhanced through exposure to the peptide, possibly combating optic nerve illnesses, stroke, and ischemic heart disease. It may potentially enhance immunological function as well.
N-Acetyl Semax Review
The Russian-synthesized Semax has been suggested to hold promise in the context of conditions including inflammation of the optic nerve, cognitive impairment, dementia, and stroke, according to researchers. Investigations purport that in addition to its depressive and anxiolytic potential, it has been investigated for its potential to strengthen the immune system. Findings imply that Semax may raise CNS levels of BDNF, serotonin, dopamine, and other neurotransmitters.
N-Acetyl Semax and Brain Structure
Functional magnetic resonance imaging purports that Semax may improve the default mode network’s performance. The regions of the brain that are typically more active while research models are not actively doing a task are collectively known as the default mode network. While little is known about this network, new data points to its potential roles in social cognition and environmental monitoring. When research models don’t have something particular in mind, it may act as a general-purpose system to monitor everything around them. As it is essential for awakening the body from its “rest” state so that it may concentrate on an event—especially one that involves social interaction—the default mode network is a crucial component of attention. Supporting the hypothesis that it is engaged in broad social awareness, the default mode network is commonly damaged in cognitive illnesses like Alzheimer’s.
While at rest, N-Acetyl Semax has been hypothesized to raise overall alertness by increasing activity in the default mode network. This causes the mind to pay more attention to its social environment. Therefore, by improving its fundamental environmental monitoring capabilities, N-acetyl Semax may make it easier for the brain to transition from a relaxed to a focused state.
Also, more connections between brain areas are often associated with more activity in the default mode network. Better problem-solving, memory, and learning capabilities have been linked to increased connections between brain regions. It is theoretically possible that Semax may increase brain function by increasing interconnectedness, even though no direct data exists to examine this claim.
N-Acetyl Semax and Stroke
Acute cerebral hypoxia, which may occur after a stroke or TBI, has been researched in Russia with N-acetyl Semax. Rat studies suggest that N-acetyl Semax may activate many CNS molecular pathways in gene transcription. More concretely, n-acetyl Semax has been hypothesized to promote alterations in the expression of twenty-four distinct genes associated with properly functioning blood vessels in the central nervous system. These genes are considered to control everything from migrating smooth muscle cells to producing new blood arteries and red blood cells. This link might shed light on the possible neuroprotective potential of N-acetyl Semax after a stroke. Seemingly, the peptide may enhance the brain’s nutrient supply, increase the likelihood that neurons will survive, and stabilize mitochondria, increasing energy output.
Using N-acetyl Semax, researchers in Russia speculated that stroke rehabilitation research models may have regained function quickly and exhibited apparently higher overall levels after presentation. Regarding increasing BDNF plasma levels, speeding functional recovery, and improving motor performance, Gusev et al. state that “early rehabilitation and administration of Semax works wonders.”
BDNF is an endogenous peptide in the brain that promotes memory and learning. The possibility exists that N-acetyl Semax may enhance neuroplasticity by activating BDNF, which may facilitate learning of previously injured areas by intact parts of the brain. In addition to its potential for resting attention and social function, Semax has been theorized to stimulate the default mode network.
N-Acetyl Semax and Cognition
Data suggests that N-acetyl Semax may improve learning and memory, which is especially intruiging to examine in research models of neurological disorders related to these areas. Canadian, American, and Chinese researchers assumed that the natural protein ACTH—the building block of N-acetyl Semax—may protect learning and memory function in epilepsy models in mice. For a long time, this protein has been the first line of defense against regression or development arrest in the context of epileptic illnesses.
Dr. Scantlebury suggests that Semax, a potent ACTH derivative, may provide properties that the original peptide may not. Although more studies are required, he does note that ACTH, even at modest concentrations, may potentially inhibit seizure-induced learning and memory impairments. This might lead to the speculation that ACTH and Semax may have nootropic qualities, meaning they may improve cognitive function when given consistently at modest levels and possibly even help with learning and memory problems caused by illness.
References
[i] I. S. Lebedeva et al., “Effects of Semax on the Default Mode Network of the Brain,” Bull. Exp. Biol. Med., vol. 165, no. 5, pp. 653–656, Sep. 2018. [PubMed]
[ii] R. B. Mars, F.-X. Neubert, M. P. Noonan, J. Sallet, I. Toni, and M. F. S. Rushworth, “On the relationship between the ‘default mode network’ and the ‘social brain,’” Front. Hum. Neurosci., vol. 6, 2012. [PMC]
[iii] E. V. Medvedeva et al., “The peptide semax affects the expression of genes related to the immune and vascular systems in rat brain focal ischemia: genome-wide transcriptional analysis,” BMC Genomics, vol. 15, p. 228, Mar. 2014. [PubMed]
[iv] E. I. Gusev, M. Y. Martynov, E. V. Kostenko, L. V. Petrova, and S. N. Bobyreva, “[The efficacy of semax in the tretament of patients at different stages of ischemic stroke],” Zh. Nevrol. Psikhiatr. Im. S. S. Korsakova, vol. 118, no. 3. Vyp. 2, pp. 61–68, 2018. [PubMed]
[v] T. I. Agapova et al., “[Effect of semax on the temporary dynamics of brain-derived neurotrophic factor and nerve growth factor gene expression in the rat hippocampus and frontal cortex],” Mol. Genet. Mikrobiol. Virusol., no. 3, pp. 28–32, 2008. [PubMed]
[vi] M. H. Scantlebury, K.-C. Chun, S.-C. Ma, J. M. Rho, and D. Y. Kim, “Adrenocorticotropic Hormone Protects Learning and Memory Function in Epileptic Kcna1-null mice,” Neurosci. Lett., vol. 645, pp. 14–18, Apr. 2017. [PubMed]
[vii] T. Deltheil et al., “Behavioral and serotonergic consequences of decreasing or increasing hippocampus brain-derived neurotrophic factor protein levels in mice,” Neuropharmacology, vol. 55, no. 6, pp. 1006–1014, Nov. 2008. [PubMed]
[viii] Ivanov, Alexander & Bobyntsev, Igor & Shepeleva, Olga & Kryukov, Alexey & Andreeva, L & Myasoedov, N. (2017). Influence of ACTG4-7-PGP (Semax) on Morphofunctional State of Hepatocytes in Chronic Emotional and Painful Stress. Bulletin of experimental biology and medicine. 163. [Research Gate]
