Epigenetics of Aggressive Behavior

Мустафин, Р. Н.; Казанцева, А.; Enikeeva, R. F.; Davydova, Yu. D.; Карунас, А. С.; Malykh, Sergey; Khusnutdinova, Elza

doi:10.1134/s1022795419090096

Cited by 6 publications

(2 citation statements)

References 95 publications

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“…A significant role of DNA methylation in telomere homeostasis has been confirmed by animal studies, which reported diminished global methylation level in subtelomeric regions providing excessive elongation of telomeres in murine embryonic stem cells with “switched-off” DNA methyltransferases [ 39 ]. Moreover, it is assumed that stress effects on the epigenome are caused by stress-sensitive transposons, which initiate the process of formation of noncoding RNAs affecting modification of histones and methylation of certain genetic loci [ 40 ].…”

Section: Discussionmentioning

confidence: 99%

Individual Differences in Relative Telomere Length in Mentally Healthy Subjects: The Effect of TERT Gene Polymorphism and Urban Residency

Казанцева

Davydova²,

Enikeeva³

et al. 2022

Russ J Genet

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The changes in the telomere length caused by the terminal underreplication in the existing literature are related to depressive disorders. However, the use of the telomere length as a biomarker of depressive states is ambiguous, which is due to the effect of various environmental factors on both the psychoemotional state and cellular aging of an organism. In order to identify the possible use of the relative telomere length (RTL) measured in peripheral blood leukocytes as a biomarker of enhanced liability to depression prior to the clinical symptoms, as well as to determine the link between telomere length, sociodemographic factors, allelic variants of the genes involved in the regulation of telomere elongation, and depression level, the association analysis of reverse transcriptase ( TERT rs7726159), telomerase RNA component ( TERC rs1317082), and the CST complex encoding protein ( OBFC1 rs2487999) gene polymorphisms was performed with RTL and depression level in mentally healthy individuals ( N = 1065) aged 18–25 years. Together with genetic variants, the examined regression models included various sociodemographic parameters as predictors. As a result of statistical analysis, we failed to observe the association between RTL and individual differences in depression level in the studied sample. Nevertheless, multiple regression analysis allowed us to construct a statistically significant model of individual variance in RTL ( P = 4.3е–4; r 2 = 0.018), which included rs7726159 in the TERT gene ( P = 0.020; β = 0.078) and such environmental predictors as age ( P = 0.001; β = –0.027) and place of residence in childhood (urban/rural area) ( P = 0.048; β = 0.063). The data obtained confirm the involvement of TERT gene variants and age in telomere length in mentally healthy individuals aged 18–25 years and indicate a negative effect of urban residency on telomere length shortening, which reflects the cellular aging of an organism.

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Section: Discussionmentioning

confidence: 99%

Individual Differences in Relative Telomere Length in Mentally Healthy Subjects: The Effect of TERT Gene Polymorphism and Urban Residency

Казанцева

Davydova²,

Enikeeva³

et al. 2022

Russ J Genet

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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: 96%

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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