{"title":"The Association of Genetic Polymorphisms and Atypical Depression in Adults: A Systematic Review.","authors":"Aysylu Galiautdinova, Iuliia Dolgopolova, Daria Troshina, Dmitry Petelin, Beatrice Volel","doi":"10.36131/cnfioritieditore20240503","DOIUrl":null,"url":null,"abstract":"<p><strong>Objective: </strong>Atypical depression (AD) is a clinical subtype of depression characterised by mood reactivity and at least two of the following features: significant weight gain/increased appetite, hypersomnia, leaden paralysis, and/or interpersonal rejection sensitivity. The role of genetics in the development of depression remains a considerable level of interest among individuals. Due to the large number of breakthrough studies in genetics, there is currently a wealth of heterogeneous data on the existence of genetic markers for depression, including AD. However, it appears that there is a gap in the literature, as we were unable to identify any systematic reviews or meta-analyses that comprehensively describe these data. Therefore, our research aims to provide high-quality, solid evidence for further studies in this area.</p><p><strong>Method: </strong>Electronic bibliographic databases (Scopus, MEDLINE) were systematically searched from inception to September 2023. We searched for any specific genetic markers that could be retrieved associated with AD. The quality of studies has been assessed by means of the Q-genie tool.</p><p><strong>Results: </strong>Nine studies meeting the inclusion criteria were selected, which appeared to link genetic polymorphisms to atypical depression. Four studies examined genetic polymorphisms associated with the serotonin transporter gene (5-HTT), three studies examined genetic polymorphisms associated with endocrine regulation, two studies considered genetic polymorphisms associated with immune and/or cellular regulation, specifically the melanin-concentrating hormone receptor 2 (MCHR2), mineralocorticoid receptor (MR), and fat mass and obesity-associated protein (FTO) genes involved in the regulation of energy balance.</p><p><strong>Conclusions: </strong>The extracted data confirm that the atypical type of major depressive disorder is heritable to a certain extent. Individual risk markers for developing this type of depression may be identified in the future.</p>","PeriodicalId":46700,"journal":{"name":"Clinical Neuropsychiatry","volume":"21 5","pages":"376-384"},"PeriodicalIF":2.0000,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11555661/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Clinical Neuropsychiatry","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.36131/cnfioritieditore20240503","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"CLINICAL NEUROLOGY","Score":null,"Total":0}
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Abstract
Objective: Atypical depression (AD) is a clinical subtype of depression characterised by mood reactivity and at least two of the following features: significant weight gain/increased appetite, hypersomnia, leaden paralysis, and/or interpersonal rejection sensitivity. The role of genetics in the development of depression remains a considerable level of interest among individuals. Due to the large number of breakthrough studies in genetics, there is currently a wealth of heterogeneous data on the existence of genetic markers for depression, including AD. However, it appears that there is a gap in the literature, as we were unable to identify any systematic reviews or meta-analyses that comprehensively describe these data. Therefore, our research aims to provide high-quality, solid evidence for further studies in this area.
Method: Electronic bibliographic databases (Scopus, MEDLINE) were systematically searched from inception to September 2023. We searched for any specific genetic markers that could be retrieved associated with AD. The quality of studies has been assessed by means of the Q-genie tool.
Results: Nine studies meeting the inclusion criteria were selected, which appeared to link genetic polymorphisms to atypical depression. Four studies examined genetic polymorphisms associated with the serotonin transporter gene (5-HTT), three studies examined genetic polymorphisms associated with endocrine regulation, two studies considered genetic polymorphisms associated with immune and/or cellular regulation, specifically the melanin-concentrating hormone receptor 2 (MCHR2), mineralocorticoid receptor (MR), and fat mass and obesity-associated protein (FTO) genes involved in the regulation of energy balance.
Conclusions: The extracted data confirm that the atypical type of major depressive disorder is heritable to a certain extent. Individual risk markers for developing this type of depression may be identified in the future.
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