Perspective - (2022) Volume 11, Issue 7
Received: 29-Jun-2022, Manuscript No. jms-22-81053;
Editor assigned: 01-Jul-2022, Pre QC No. P-81053;
Reviewed: 14-Jul-2022, QC No. Q-81053;
Revised: 18-Jul-2022, Manuscript No. R-81053;
Published:
25-Jul-2022
, DOI: 10.37421/ 2167-0943.2022.11.286
Citation: Modabbernia, Amirhossein. “Melatonin's Role in Schizophrenia." J Metabolic Synd 11 (2022): 286.
Copyright: © 2022 Modabbernia A. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Schizophrenia is a long-term mental illness that affects memory, thought, perception and volition among other cognitive processes. The multifactorial biological etiology of schizophrenia is still under investigation. Since the early twentieth century, schizophrenia has been linked to melatonin. There have been two distinct approaches taken in schizophrenia research involving melatonin. The utilization of melatonin as a biological marker is the basis for the first strategy. Melatonin's clinical uses as a medication are the focus of the second strategy. Both aspects of using melatonin are looked at in this paper. Its clinical use in schizophrenia is underlined [1].
There is now a substantial body of research linking schizophrenia to prenatal events such as obstetric complications or maternal infection during pregnancy, despite the fact that the symptoms of schizophrenia typically appear in adolescence and early adulthood. As a result, perinatal and early postnatal drug administration and/or environmental manipulation are used in developmental animal models of schizophrenia. The children are then studied throughout their development. Neonatal lesions of the rat ventral hippocampus on postnatal day 7 were one of the first developmental preparations used to study schizophrenia. These lesions were caused by local injection of the excitotoxin ibotenic acid or temporary inactivation with tetrodotoxin. Arrays of abnormalities that are consistent with schizophrenia emerge at various times after puberty, similar to the typical onset of schizophrenia in late adolescence or early adulthood, but not from similar lesions performed in early adulthood. Models of schizophrenia have also utilized postnatal developmental manipulations like the administration of glutamate receptor agonists and antagonists, postweaning stress, or postweaning social isolation. Notably, adult behavioral changes caused by postnatal social isolation include spontaneous locomotor hyperactivity, enhanced response to novelty, sensorimotor gating deficits, cognitive impairment and increased anxiety and aggression [2].
We used NLP to do a large-scale literature data mining with the help of Pathway Studio to find common genes that were SCZ's downstream targets and MI's up-regulators. That is, a relationship between SCZ and MI was found between each gene, which was found to be influenced by SCZ and also regulating MI. In the supplementary material SCZ_MIRef4GeneticPathway, there were at least three independent supporting references for each identified relationship. These references included the title, DOI/PMID and the sentences in which the relationship was identified. MedScan, an NLP-based literature data mining tool, was used to carry out the procedure. Over 24 million PubMed abstracts and 3. 5 million Elsevier and 3rd party full-text papers were the subject of the data mining. NLP technology was used to extract facts from the literature and at least three supporting references were used to build each relationship or edge. To get rid of relationships that weren't reliable and relationships with polarities that weren't specific, a manual quality control procedure was used. In this context, the term "unreliable relationships" refers to those with sentences that do not match, which were false positives generated by the NLP technique [3].
Additionally, administration time may play a significant role in advancing melatonin's circadian rhythm. A meta-analysis found that administration at 18:00 or 20:00 h may be most effective, though this may vary from person to person. Based on the phase-response curve, the optimal administration time would be three hours prior to the dim-light melatonin onset (DLMO). Consequently, depending on the purpose of melatonin supplements, it is necessary to apply both an appropriate dose and an appropriate dosing time in order to more effectively correct sleep or circadian abnormalities in psychiatric disorders. As a chronobiotic, low-dose melatonin (less than 1 mg) may be effective in advancing sleep and circadian rhythms in previous studies. The dose had an impact on the phase-response curve. The most effective time to advance the rhythm may be two hours before DLMO at doses as low as 1 mg. On the other hand, the best time to administer high doses like 3 mg might be 5 hours before DLMO. High doses of melatonin may not be beneficial for advancing the melatonin rhythm because the dosage-dependent phaseresponse curve differs [4,5].
We quantitatively reviewed the effectiveness of various anti-inflammatory medications in reducing the severity of symptoms in schizophrenia patients in this meta-analysis. In addition to antipsychotic treatment, data from 56 studies using 16 different agents could be included. In a meta-analysis of at least two studies, aspirin, estrogens, minocycline and NAC outperformed placebo significantly, while pioglitazone, piracetam and WSE were only significant in one study. Pregnenolone, varenicline, bexarotene, celecoxib, davunetide, dextromethorphan, fatty acids and statins had no significant beneficial effects.
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Journal of Metabolic Syndrome received 48 citations as per Google Scholar report