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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.
for the first time, we explored how environmental adversities and GRIN2B genetic variants influence children's cognitive abilities and behavioral problems.
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.
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).
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.
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.
A multigroup path analysis was employed in a general adolescent population sample of a 5-year follow-up study.
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.
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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