The Role of Epigenetic Factors in the Development of Depressive Disorders

Мустафин, Р. Н.; Enikeeva, R. F.; Davydova, Yu. D.; Khusnutdinova, Elza

doi:10.1134/s1022795418120104

Cited by 3 publications

(2 citation statements)

References 80 publications

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“…The studies of epigenetic factors including methylation and modifications of histones, microRNAs, and long non-coding RNAs examined in details in the previous review (Mustafin et al, 2018) are expected to make a significant contribution to unravel the nature of DDs. The role of gene-environmental interactions, ethnicity-geographic and socio-cultural factors in manifestation of depressive symptoms via epigenetic mechanisms of gene expression regulation representing a particular interest in further research in this field could not be excluded.…”

Section: Resultsmentioning

confidence: 99%

Genetic basis of depressive disorders

Давыдова¹,

Enikeeva²,

Казанцева³

et al. 2019

Vestn. VOGiS

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Depression is a common mental disorder being one of the main causes of disability and mortality worldwide. Despite an intensive research during the past decades, the etiology of depressive disorders (DDs) remains incompletely understood; however, genetic factors are significantly involved in the liability to depression. The present review is focused on the studies based on a candidate gene approach, genome-wide association studies (GWAS) and whole exome sequencing (WES), which previously demonstrated associations between gene polymorphisms and DDs. According to the first approach, DD development is affected by serotonergic (TPH1, TPH2, HTR1A, HTR2A, and SLC6A4), dopaminergic (DRD4, SLC6A3) and noradrenergic (SLC6A2) system genes, and genes of enzymatic degradation (MAOA, COMT). In addition, there is evidence of the involvement of HPA-axis genes (OXTR, AVPR1A, and AVPR1B), sex hormone receptors genes (ESR1, ESR2, and AR), neurotrophin (BDNF) and methylenetetrahydrofolate reductase (MTHFR) genes, neuronal apoptosis (CASP3, BCL-XL, BAX, NPY, APP, and GRIN1) and inflammatory system (TNF, CRP, IL6, IL1B, PSMB4, PSMD9, and STAT3) genes in DD development. The results of the second approach (GWAS and WES) revealed that the PCLO, SIRT1, GNL3, GLT8D1, ITIH3, MTNR1A, BMP5, FHIT, KSR2, PCDH9, and AUTS2 genes predominantly responsible for neurogenesis and cell adhesion are involved in liability to depression. Therefore, the findings discussed suggest that genetic liability to DD is a complex process, which assumes simultaneous functioning of multiple genes including those reported previously, and requires future research in this field.

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Section: Resultsmentioning

confidence: 99%

Genetic basis of depressive disorders

Давыдова¹,

Enikeeva²,

Казанцева³

et al. 2019

Vestn. VOGiS

Self Cite

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“…The miR-222 and miR-92 provide neurite growth via negative regulation of neuronal growth inhibitor, PTEN, and via activating CREB expression and phosphorylation [87]. The analysis of published data also demonstrated the role of epigenetic factors in development of depressive disorders [88], aggressive behavior [89], and aging [90]. This indicates the necessity of studying noncoding RNAs within brain functioning owing to the possibility of affecting both cognitive abilities and socially significant deviations in behavior and mental health.…”

Section: The Role Of Noncoding Rnas In Cognitive Developmentmentioning

confidence: 97%

Genetic Mechanisms of Cognitive Development

et al. 2020

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The results of large-scale meta-analyses of GWAS and genetic association studies demonstrated the role of allelic variants of a large number of genes in the development of cognitive abilities. Many of the identified genes are expressed in the brain and are involved in the pathogenesis of nervous system diseases. It has been shown that the summarized genetic effect for various cognitive abilities is no more than 50%. For certain genes, such as BDNF, DRD2, FNBP1L, PDE1C, PDE4B, and PDE4D, related to the regulation of neurogenesis and synaptic plasticity, associations with specific cognitive abilities were revealed. We assume the prospect of using the obtained results for the targeted effect in order to improve human cognitive abilities. This review describes DNA methylation, histone acetylation, expression of specific noncoding RNAs during brain functioning, and the development of individual differences in cognitive abilities. The revealed epigenetic mechanisms suggest the methods of reversible correction of cognitive functioning both in nonclinical forms and pathological states.

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Risk of Depression after Radiation

Zasukhina,

Maximova

2023

Biol Bull Russ Acad Sci

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The Role of Epigenetic Factors in the Development of Depressive Disorders

Cited by 3 publications

References 80 publications

Genetic basis of depressive disorders

Genetic basis of depressive disorders

Genetic Mechanisms of Cognitive Development

Risk of Depression after Radiation

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