The clinical term “depression” has long been considered to result from an imbalance in serotonin, norepinephrine, and dopamine neurotransmitters. In addition to monoamine oxidase inhibitors (MAOIs), serotonin-norepinephrine reuptake inhibitors (SNRIs), tricyclic anti-depressants, and compounds that target norepinephrine and dopamine levels, selective serotonin reuptake inhibitors (SSRIs) increased as a consequence of the “chemical imbalance” idea. These sustances were promoted as 80-90% effective against depression and associated disorders in the early 1990s.
With recent research, scientific professionals have formed a new hypothesis that SSRIs and other compounds with comparable mechanisms of action may not induce enough of a chemical impact, and other revolutionary research areas have taken shape, including the further study of research peptides and electroconvulsive action, among others.
The etiology and pathophysiology of depression probably include neuropeptides or active peptides in the central nervous system. Available research suggests that peptides like Vasopressin, Galanin, and neuropeptide Y may be important in regulating monoaminergic receptor transmission. Serotonin and dopamine are only two examples of neurotransmitters presumably regulated at the molecular level by peptides. Incorrect chemical control and signaling, rather than a “chemical imbalance,” is considered to be the root of depression manifestation.
Many neuropsychiatric symptoms may be attributed to a malfunction of certain receptors or their ligands, and data suggests that neuropeptide systems may play a role in this. Several neuropeptide systems, such as arginine-vasopressin, cholecystokinin, corticotropin-releasing factor, and neuropeptide Y, have been linked to schizophrenia.
Studies suggest that electroconvulsive therapy (ECT) may affect some peptide levels in the brain and provides more data on the possible correlation between peptides and depression. Although electroconvulsive therapy (ECT) may effectively manage mood disorders, including depression, its usage is typically restricted to refractory, severe cases due to its associated risks. The true advantage of ECT appears to lie in its capacity to assist the brain in managing neuropeptides, with studies showing that ECT affects a range of peptides, including neuropeptide Y, galanin, and somatostatin.
Ghrelin
Studies suggest that the hunger hormone Ghrelin may aid in the alleviation of depressive brain activity. Increased cortisol levels are associated with an increase in this peptide, which has been hypothesized to control growth hormone and energy balance. High amounts of the stress hormone cortisol have been linked to depression, but it is not entirely obvious that cortisol is to blame.
Reducing depressive behavior and hypomotility in rats by lowering cortisol levels has been linked to stimulation of the ghrelin receptor (also known as the growth hormone secretagogue receptor). It has also been speculated that tryptophan metabolism may be affected when Ghrelin production is reduced in mice. Many neurotransmitters thought to play a role in depression’s pathophysiology are considered to depend on tryptophan as an intermediate step in their biosynthesis.
Peptide research within the context of depression is still in its infancy, and more preclinical investigations is expected. However, there is encouraging data from studies on animal models of depression and anxiety suggesting that particular peptides may potentially produce quantifiable and statistically significant improvement. Some examples of peptides researched within this context are discussed below.
Pinealon Peptide
Pinealon is a short-chain peptide that has been hypothesized to impact gene expression by interacting with DNA. Animal studies have purported that under the influence of supplemental Pinealon, behavior may be altered and significant positive impacts may be seen within circadian rhythm function. Pinealon has suggested some potential in animal models of depression, which is not surprising given the strong correlation that researchers have suggested between sleep and depression chemical production imbalances.
Data suggests that Pinealon may increase 5-tryptophan hydroxylase expression in the brain. This enzyme may affect brain serotonin levels because of its central function in serotonin biosynthesis. Furthermore, Pinealon has been speculated to lessen neuropsychiatric signs of disturbed or inadequate sleep.
Selank Peptide
Both anxiety and depression are commonly diagnosed together because of how closely they are connected. Results from studies of research models of anxiety and depression point to a role for the inflammatory cytokine IL-6 in both disorders. When nerve pain, weariness, headache, heart palpitations, and high blood pressure accompany the symptoms of depression and complicate therapy, it seems that IL-6 may potentially play a significant role in models of anxiety-asthenic disorder and other psychosomatic diseases.
Semax Peptide
Studies have suggested that research models of depression have exhibited lower levels of BDNF (brain-derived neurotrophic factor). BDNF is considered to be crucial in developing, surviving, and maintaining neurons and synapses. Abnormalities in BDNF levels and BDNF receptors have been closely connected to depression. At the same time, it is unclear whether reduced BDNF levels are a result or cause of depression.
Scientific studies have explored the impact of increasing BDNF levels. It has been hypothesized that the rat brain (particularly the basal forebrain) may respond to Semax, a short synthetic derivative of adrenocorticotrophic hormone (ACTH), by increasing its levels of brain-derived neurotrophic factor (BDNF. Semax has also been studied for its potential function within the context of attention-deficit hyperactivity disorder (ADHD).
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References
[i] J. C. Fournier et al., “Antidepressant Drug Effects and Depression Severity: A Patient-Level Meta-analysis,” JAMA, vol. 303, no. 1, pp. 47–53, Jan. 2010, doi: 10.1001/jama.2009.1943.
[ii] V. Madaan and D. R. Wilson, “Neuropeptides: relevance in treatment of depression and anxiety disorders,” Drug News Perspect., vol. 22, no. 6, pp. 319–324, Aug. 2009, doi: 10.1358/dnp.2009.22.6.1395255.
[iii] R. Cáceda, B. Kinkead, and C. B. Nemeroff, “Involvement of neuropeptide systems in schizophrenia: human studies,” Int. Rev. Neurobiol., vol. 78, pp. 327–376, 2007, doi: 10.1016/S0074-7742(06)78011-4.
[iv] A. A. Mathé, “Neuropeptides and electroconvulsive treatment,” J. ECT, vol. 15, no. 1, pp. 60–75, Mar. 1999.
[v] ]Y.-L. Liu et al., “Meranzin Hydrate Improves Depression-Like Behaviors and Hypomotility via Ghrelin and Neurocircuitry,” Chin. J. Integr. Med., Jul. 2022
[vi] E. Tuchaai et al., “Deletion of ghrelin alters tryptophan metabolism and exacerbates experimental ulcerative colitis in aged mice,” Exp. Biol. Med. Maywood NJ, p. 15353702221110648, Jul. 2022, doi: 10.1177/15353702221110647.
[vii] M. V. Masule et al., “Ghrelin mediated regulation of neurosynaptic transmitters in depressive disorders,” Curr. Res. Pharmacol. Drug Discov., vol. 3, p. 100113, 2022, doi: 10.1016/j.crphar.2022.100113.
[viii] R. H. Ehrensing and A. J. Kastin, “Dose-related biphasic effect of prolyl-leucyl-glycinamide (MIF-I) in depression,” Am. J. Psychiatry, vol. 135, no. 5, pp. 562–566, May 1978, doi: 10.1176/ajp.135.5.562.
