Posters
Presenting Author Academic/Professional Position
Jefferson Tait
Academic Level (Author 1)
Medical Student
Academic Level (Author 2)
Medical Student
Academic Level (Author 3)
Medical Student
Academic Level (Author 4)
Medical Student
Academic Level (Author 5)
Medical Student
Discipline Track
Clinical Science
Abstract Type
Research/Clinical
Abstract
Background: The use of peptides as an alternative treatment for neurological disease is an emerging practice that has had tremendous success. Semax, a synthetic heptapeptide derived from adrenocorticotropic hormone (ACTH 4–10), is well known and used clinically in Russia and Eastern Europe for ischemic stroke therapy. Moreover, Semax has also been reported to modulate monoaminergic systems. Because Parkinson’s disease (PD) involves the loss of dopaminergic neurons, Semax’s neuromodulatory properties make it a potential candidate for the treatment of Parkinson's. Here, we hope to evaluate whether Semax could be an alternative therapy for PD by reviewing evidence on its effects on dopamine release, locomotor behavior and non‑motor symptoms.
Methods: A qualitative literature review was conducted using PubMed and SCIRP. We included peer-reviewed rodent studies that measured dopamine, serotonin, or locomotor outcomes after Semax administration, alone or in combination with psychostimulants.
Results: While nearly all studies agree that Semax can improve anxiety, prior work on the effect of Semax with different types of PD-like rat models did not significantly change the striatal dopamine levels or improve locomotor activity. One study showed that at higher doses (.2 mg/kg), a significant increase in motor performance was seen. In another study, no changes in tissue or extracellular dopamine were observed upon the administration of Semax alone. However, when Semax was given 20 minutes before d‑amphetamine, it markedly amplified d‑amphetamine–induced dopamine release and locomotor activity.
Conclusion: Overall, current pre‑clinical evidence suggests that Semax could influence serotonergic and dopaminergic systems, potentially benefiting non‑motor and motor symptoms of PD. However, low doses of Semax does not improve motor deficits in animal models and no clinical trials have tested its efficacy in human PD patients. Further research is needed before Semax can be considered a viable treatment for Parkinson’s disease.
Presentation Type
Poster
Recommended Citation
Tait, Jefferson; Karkoutly, Mohammad Yaman; Rakay, David; and Aquino, Edurado, "Semax for Parkinson’s Neuroprotection: A Qualitative Review of Preclinical Evidence" (2025). Research Colloquium. 50.
https://scholarworks.utrgv.edu/colloquium/2025/posters/50
Included in
Semax for Parkinson’s Neuroprotection: A Qualitative Review of Preclinical Evidence
Background: The use of peptides as an alternative treatment for neurological disease is an emerging practice that has had tremendous success. Semax, a synthetic heptapeptide derived from adrenocorticotropic hormone (ACTH 4–10), is well known and used clinically in Russia and Eastern Europe for ischemic stroke therapy. Moreover, Semax has also been reported to modulate monoaminergic systems. Because Parkinson’s disease (PD) involves the loss of dopaminergic neurons, Semax’s neuromodulatory properties make it a potential candidate for the treatment of Parkinson's. Here, we hope to evaluate whether Semax could be an alternative therapy for PD by reviewing evidence on its effects on dopamine release, locomotor behavior and non‑motor symptoms.
Methods: A qualitative literature review was conducted using PubMed and SCIRP. We included peer-reviewed rodent studies that measured dopamine, serotonin, or locomotor outcomes after Semax administration, alone or in combination with psychostimulants.
Results: While nearly all studies agree that Semax can improve anxiety, prior work on the effect of Semax with different types of PD-like rat models did not significantly change the striatal dopamine levels or improve locomotor activity. One study showed that at higher doses (.2 mg/kg), a significant increase in motor performance was seen. In another study, no changes in tissue or extracellular dopamine were observed upon the administration of Semax alone. However, when Semax was given 20 minutes before d‑amphetamine, it markedly amplified d‑amphetamine–induced dopamine release and locomotor activity.
Conclusion: Overall, current pre‑clinical evidence suggests that Semax could influence serotonergic and dopaminergic systems, potentially benefiting non‑motor and motor symptoms of PD. However, low doses of Semax does not improve motor deficits in animal models and no clinical trials have tested its efficacy in human PD patients. Further research is needed before Semax can be considered a viable treatment for Parkinson’s disease.
