학술논문
Heritability and genome-wide analyses of problematic peer relationships during childhood and adolescence
Original Investigation
Original Investigation
Document Type
Academic Journal
Author
Source
Human Genetics. June 2015, Vol. 134 Issue 6, p539, 13 p.
Subject
Language
English
ISSN
0340-6717
Abstract
Author(s): Beate St Pourcain[sup.1] [sup.2] [sup.3] [sup.4] , C. M. A. Haworth[sup.5] [sup.6] , O. S. P. Davis[sup.6] [sup.7] , Kai Wang[sup.8] [sup.9] , Nicholas J. Timpson[sup.1] [sup.4] , David [...]
Peer behaviour plays an important role in the development of social adjustment, though little is known about its genetic architecture. We conducted a twin study combined with a genome-wide complex trait analysis (GCTA) and a genome-wide screen to characterise genetic influences on problematic peer behaviour during childhood and adolescence. This included a series of longitudinal measures (parent-reported Strengths-and-Difficulties Questionnaire) from a UK population-based birth-cohort (ALSPAC, 4-17 years), and a UK twin sample (TEDS, 4-11 years). Longitudinal twin analysis (TEDS; N [less than or equal to] 7,366 twin pairs) showed that peer problems in childhood are heritable (4-11 years, 0.60 < twin-h.sup.2 [less than or equal to] 0.71) but genetically heterogeneous from age to age (4-11 years, twin-r.sub.g = 0.30). GCTA (ALSPAC: N [less than or equal to] 5,608, TEDS: N [less than or equal to] 2,691) provided furthermore little support for the contribution of measured common genetic variants during childhood (4-12 years, 0.02 < GCTA-h.sup.2(Meta) [less than or equal to] 0.11) though these influences become stronger in adolescence (13-17 years, 0.14 < GCTA-h.sup.2(ALSPAC) [less than or equal to] 0.27). A subsequent cross-sectional genome-wide screen in ALSPAC (N [less than or equal to] 6,000) focussed on peer problems with the highest GCTA-heritability (10, 13 and 17 years, 0.0002 < GCTA-P [less than or equal to] 0.03). Single variant signals (P [less than or equal to] 10.sup.-5) were followed up in TEDS (N [less than or equal to] 2835, 9 and 11 years) and, in search for autism quantitative trait loci, explored within two autism samples (AGRE: N.sub.Pedigrees = 793; ACC: N.sub.Cases = 1,453/N.sub.Controls = 7,070). There was, however, no evidence for association in TEDS and little evidence for an overlap with the autistic continuum. In summary, our findings suggest that problematic peer relationships are heritable but genetically complex and heterogeneous from age to age, with an increase in common measurable genetic variation during adolescence.
Peer behaviour plays an important role in the development of social adjustment, though little is known about its genetic architecture. We conducted a twin study combined with a genome-wide complex trait analysis (GCTA) and a genome-wide screen to characterise genetic influences on problematic peer behaviour during childhood and adolescence. This included a series of longitudinal measures (parent-reported Strengths-and-Difficulties Questionnaire) from a UK population-based birth-cohort (ALSPAC, 4-17 years), and a UK twin sample (TEDS, 4-11 years). Longitudinal twin analysis (TEDS; N [less than or equal to] 7,366 twin pairs) showed that peer problems in childhood are heritable (4-11 years, 0.60 < twin-h.sup.2 [less than or equal to] 0.71) but genetically heterogeneous from age to age (4-11 years, twin-r.sub.g = 0.30). GCTA (ALSPAC: N [less than or equal to] 5,608, TEDS: N [less than or equal to] 2,691) provided furthermore little support for the contribution of measured common genetic variants during childhood (4-12 years, 0.02 < GCTA-h.sup.2(Meta) [less than or equal to] 0.11) though these influences become stronger in adolescence (13-17 years, 0.14 < GCTA-h.sup.2(ALSPAC) [less than or equal to] 0.27). A subsequent cross-sectional genome-wide screen in ALSPAC (N [less than or equal to] 6,000) focussed on peer problems with the highest GCTA-heritability (10, 13 and 17 years, 0.0002 < GCTA-P [less than or equal to] 0.03). Single variant signals (P [less than or equal to] 10.sup.-5) were followed up in TEDS (N [less than or equal to] 2835, 9 and 11 years) and, in search for autism quantitative trait loci, explored within two autism samples (AGRE: N.sub.Pedigrees = 793; ACC: N.sub.Cases = 1,453/N.sub.Controls = 7,070). There was, however, no evidence for association in TEDS and little evidence for an overlap with the autistic continuum. In summary, our findings suggest that problematic peer relationships are heritable but genetically complex and heterogeneous from age to age, with an increase in common measurable genetic variation during adolescence.