Research suggests Semax may improve the performance of the “default mode network,” as suggested by functional magnetic resonance imaging.
The default mode network is a group of brain areas that is considered to be more active while the test subject is inert than when they are engaged in an activity. Although not fully understood, this network may contribute to social cognition and environmental monitoring, according to current studies. It may be a catch-all method for keeping tabs on the environment while an organism is not actively exhibiting attentiveness. As an organism might not be paying attention—especially something that requires interaction—until it has been roused from a “rest” state, the default mode network may be a crucial component of attention. The default mode network is often impaired in cognitive disfunctions, contributing to the theory that it may play a role in an organism’s awareness.
Studies suggest Semax may improve resting arousal by increasing activity in the default mode network. As a result, the organism may pay more attention to its surroundings, especially in social situations. In other words, Semax may facilitate the brain’s transition from a resting to a focused state by increasing the brain’s fundamental environmental monitoring activities.
It’s also worth noting that more communication across brain areas often correlates with higher default mode network activity levels. Improved problem-solving, memory, and creativity have all been linked to increased connection. The possibility that Semax may enhance global brain function by increasing interconnection exists despite the lack of empirical evidence for this action.
Semax and Stroke
Studies suggest the impact of acute cerebral hypoxia, such as that caused by a stroke or severe brain injury, may be mitigated with Semax. Semax, as speculated by rat studies, may activate many molecular processes involved in CNS gene transcription. Scientists hypothesize Semax may directly impact the expression of 24 genes involved in brain and spinal cord blood vessel function. Everything from the production of red blood cells to the development of new blood vessels is considered to be controlled by this set of genes. Research suggests that this association might explain the potential neuroprotective action of Semax after stroke. The peptide seems to increase neuron survival, stabilize mitochondria, and, by extension, energy output and boost brain nutrition.
Clinical studies on test subjects following a stroke and undergoing rehabilitation have suggested that using Semax may increase the pace at which function recovers and the total level of function at the end. Researchers Gusev et al. say that “early rehabilitation of Semax may increase BDNF plasma levels, speed functional recovery, and improve motor performance.”
Scientists hypothesize the brain peptide BDNF may promote memory and learning. Semax may enhance neuroplasticity by increasing levels of brain-derived neurotrophic factor, making it simpler for brain areas to pick up the slack for injured ones when learning new skills. As previously speculated, Semax may also engage the default mode network, considered essential for focused resting attention and social interaction.
Semax and Gene Expression
Researchers speculate alterations in brain gene expression possibly caused by Semax may not be exclusive to the context of stroke. Studies suggest that Semax, when presented to rats, may affect many genes in the brain’s hippocampus and prefrontal cortex. The frontal cortex is considered crucial for focused attention, planning, and organizing information, and the hippocampus may play a crucial role in memory and learning. Researchers hypothesize that within 20 minutes of Semax presentation, gene expression appears in both organs, with a notable impact on nerve growth factor (NGF) and BDNF.
Semax and the Brain
Research suggests Semax is based on a natural protein called ACTH, which may preserve learning and memory function in mice models of epilepsy, according to studies conducted in Canada, the United States, and China [vi]. The protein has been utilized for quite some time in research as a potential defense against developmental stoppage or regression in mitigating the action of epileptic diseases.
Dr. Scantlebury suggests that Semax, a ACTH derivative, may have potential properties not present with the original peptide. Though additional study is needed, he notes that ACTH, even in modest quantities, may protect against learning and memory deficits in the presence of a seizure. This might imply that ACTH and Semax may have nootropic properties, improving cognitive function when used routinely and compensating for learning and memory deficiencies when illness is present.
More investigation is required to explore the peptide’s potential in scientific research, and these studies must continue. Only academic and scientific institutions are allowed to use Semax peptides. If you are a licensed professional interested in buying peptides for your clinical studies, click here. Please note that none of the items mentioned are approved for human or animal consumption. Laboratory research chemicals are only for in-vitro and in-lab use. Any kind of physical introduction is illegal. Only authorized academics and working professionals may make purchases. The content of this article is intended only for instructional purposes.
[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]