SNP‐Based Heritability Estimates of Common and Specific Variance in Self‐ and Informant‐Reported Neuroticism Scales. Issue 6 (13th February 2017)

• Record Type: Journal Article
• Authors: Realo, Anu; van der Most, Peter J.; Allik, Jüri; Esko, Tõnu; Jeronimus, Bertus F.; Kööts‐Ausmees, Liisi; Mõttus, René; Tropf, Felix C.; Snieder, Harold; Ormel, Johan
• Is Part Of: Journal of personality. Volume 85:Issue 6(2017)
• Page Start: 906
• Page End: 919
• Publication Date: 2017-02-13
• Subjects: Neuroticism -- GREML‐GCTA -- SNP‐based heritability -- self‐ versus informant reports -- sum versus residual scores; Psychology -- Periodicals; Character -- Periodicals; Personality -- Periodicals; Personality; 155.2
• DOI: 10.1111/jopy.12297
• Languages: English
• ISSNs: 0022-3506

Abstract

Abstract: Objective: Our study aims to estimate the proportion of the phenotypic variance of Neuroticism and its facet scales that can be attributed to common single‐nucleotide polymorphisms (SNPs) in two adult populations from Estonia (EGCUT; N = 3, 292) and the Netherlands (Lifelines; N = 13, 383). Method: Genomic‐relatedness‐matrix restricted maximum likelihood (GREML) using genome‐wide complex trait analysis (GCTA) software was employed. To build upon previous research, we used self‐ and informant reports of the 30‐facet NEO personality inventories and analyzed both the usual sum scores and the residual facet scores of Neuroticism. Results: In the EGCUT cohort, the proportion of phenotypic variance explained by the additive effects of common genetic variants in self‐ and informant‐reported Neuroticism domain scores was 15.2% ( p = .070, SE = .11) and 6.2% ( p = .293, SE = .12), respectively. The SNP‐based heritability estimates at the level of Neuroticism facet scales differed greatly across cohorts and modes of measurement but were generally higher (a) for self‐ than for informant reports, and (b) for sum than for residual scores. Conclusions: Our findings indicate that a large proportion of the heritability of Neuroticism is not captured by additive genetic effects of common SNPs, with some evidence for Gene × Environment interaction across cohorts.