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Epigenetics hypothesizes a crucial link between postnatal risk factors, individual response to stress, DNA methylation and psychiatric symptomatology changes during life.
Objectives
We analyzed methylation within two gene exons: NR3C1 and SLC6A4, which are involved in responses to environmental stressors. We investigated the relationship between methylation, postnatal risk factors and psychopathology assessed by Child Behavior Checklist (CBCL) in our help-seeking sample evaluated in infancy (W1), preadolescence (W2) and adult life (W3).
Methods
Postnatal risk factors data were collected at W1 in 205 clinical subjects (156 M, 49 F; age=9,13±1,95). The CBCL scores were collected at W1 and W2 (W2 age=14,52±2,12). Data regarding methylation were collected at W2. At W3 we are also collecting clinical scores. A Spearman correlation coefficient was calculated between methylation percentage and clinical data at W2. The externalizing and internalizing trajectories were evaluated through repeated measure ANOVA with postnatal risk factors (presence/absence) as between-groups factor.
Results
Significant associations were found between methylation and internalizing and total clinical scores (Table 1). The rm-ANOVA results showed a significant interaction between the CBCL internalizing score and presence/absence of postnatal risk, with higher internalizing problems in subjects that were exposed to postnatal risk factors. This effect was significant at W2 but not at W1 (Figure 1).
Conclusions
Psychopathological symptoms trajectories could depend on epigenetics and early environmental risk factors. Further analyses will address a Linear Discriminant Analysis to proceed to a machine learning oriented approach.
it is well established that adversities and GRIN2B genetic variants (encoding NMDAR GluN2B subunit) are independently associated with behavioral and cognitive impairments in childhood. However, a high proportion of children exposed to risk have good, long-term outcomes.
Objectives
for the first time, we explored how environmental adversities and GRIN2B genetic variants influence children's cognitive abilities and behavioral problems.
Aims
we adopted a gene-by-environment interaction (GxE) approach, to identify children with an unfavorable developmental outcome with the potential of better informing the understanding of susceptibility to developmental disorders.
Methods
6 SNPs of GRIN2B were genotyped in 625 children aged 6-11 years from an Italian community-based sample. The interactive effect of GRIN2B variants with 4 measures of adversities (low socioeconomic status - SES, preterm delivery, maternal smoking, absence of breastfeeding) was investigated upon cognitive abilities (vocabulary, block design, forward/backward digit spans of Wechsler's Intelligence Scale, and Rey Figure test) and parents-rated behavioral problems (Child Behavior Checklist/6-18).
Results
rs5796555 x gestational age interaction (p= .00145) influenced cognition, with lower IQ memory among children in the ‘A/A genotype and ≤ 36 gestational age’ group, compared to all other groups. Rs2268119 x SES interaction (p= .00008) influenced behavior, with more attention problems among children in the ‘either A/T or T/T genotype and low SES’ group, compared to all other groups.
Conclusions
GRIN2B targets children with the worst outcome in memory and attention functioning among children exposed to environmental adversities. Identification of children with the highest risk may prompt cost-effective preventive/treatment strategies.
Many studies of various stress reactive phenotypes suggest that 5-HTTLPR short allele carriers (S-carriers) are characterised by the stable trait of negative affectivity that is converted to psychopathology only under conditions of stress. In this study, we examined the moderating role of the 5-HTTLPR on the relationship between two objective chronic risk factors, i.e. socioeconomic status (SES) and family structure, and internalising symptoms across adolescence.
Methods.
A multigroup path analysis was employed in a general adolescent population sample of a 5-year follow-up study.
Results.
Internalising problems were significantly more stable in the S-carriers. The focus on the main dimensions of internalising problems, i.e. anxiety and depression, revealed two different developmental patterns. In the S-carriers Anxiety problems seemed to be more stable and to predict a possible evolution towards the development of Depressive problems. In the long allele homozygotes (LL-subjects) the anxiety trait was significantly less stable, and, in late-adolescence, seemed to be significantly predicted by SES, suggesting a possible gene–environment interaction (G × E). Family structure seemed to play a role in a G × E perspective only until early-adolescence, while during late-adolescence SES seemed to play a pivotal role in interaction with 5-HTTLPR, with the S-allele playing a protective role.
Conclusions.
Future models of the developmental link between environmental adversities and internalising behaviour therefore need to consider that the effect of G × E interaction, may be associated with internalising behaviour via different mechanisms during different time frames and that shifts in the strength of this effect should be expected across development.
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