The heritability of general cognitive ability increases linearly from childhood to young adulthood

Haworth, Claire M. A.; Wright, Margaret J.; Luciano, Michelle; Martin, Nicholas G.; Geus, Eco J. C. de; Beijsterveldt, Catharina E. M. van; Bartels, Meike; Posthuma, Daniëlle; Boomsma, Dorret I.; Davis, Oliver S. P.; Kovas, Yulia; Corley, Robin P.; DeFries, John C.; Hewitt, John K.; Olson, Richard K.; Rhea, Sa; Wadsworth, Sally J.; Iacono, William G.; McGue, Matthew; Thompson, Lee A.; Hart, Sara A.; Petrill, Stephen A.; Lubinski, David; Plomin, Robert

doi:10.1038/mp.2009.55

Cited by 546 publications

(473 citation statements)

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“…This is a demonstration of the relevance of genes implicated in monogenic disorders of cognitive ability to continuous variability in intelligence. Despite the high heritability of intelligence, 12,28,37,38 the progress in the identification of loci consistently associated with variation in its normal range has thus far been limited. 15,17,[38][39][40][41][42] Exceptions are the apolipoprotein E (APOE) gene at older ages 43 and formin binding protein 1-like (FNBP1L), the latter having recently been shown to be associated with both childhood and adulthood intelligence.…”

Section: Discussionmentioning

confidence: 99%

Intelligence: shared genetic basis between Mendelian disorders and a polygenic trait

et al. 2015

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Multiple inquiries into the genetic etiology of human traits indicated an overlap between genes underlying monogenic disorders (eg, skeletal growth defects) and those affecting continuous variability of related quantitative traits (eg, height). Extending the idea of a shared genetic basis between a Mendelian disorder and a classic polygenic trait, we performed an association study to examine the effect of 43 genes implicated in autosomal recessive cognitive disorders on intelligence in an unselected Dutch population (N = 1316). Using both single-nucleotide polymorphism (SNP)-and gene-based association testing, we detected an association between intelligence and the genes of interest, with genes ELP2, TMEM135, PRMT10, and RGS7 showing the strongest associations. This is a demonstration of the relevance of genes implicated in monogenic disorders of intelligence to normal-range intelligence, and a corroboration of the utility of employing knowledge on monogenic disorders in identifying the genetic variability underlying complex traits.

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Section: Discussionmentioning

confidence: 99%

Intelligence: shared genetic basis between Mendelian disorders and a polygenic trait

et al. 2015

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“…High heritability has been observed in twin‐based studies for various neurocognitive traits, including episodic memory, working memory and general cognitive ability [Ando J et al, 2001; Haworth et al, 2010; Owens SF et al, 2011]. Similarly, molecular genetic studies have predicted increased heritability estimates for general cognitive ability in the general population by considering the additive effects of thousands common genetic markers in the human genome [Plomin R et al, 2013; Benyamin B et al, 2014].…”

Section: Introductionmentioning

confidence: 99%

Common genetic variation and schizophrenia polygenic risk influence neurocognitive performance in young adulthood

Hatzimanolis

Bhatnagar

Moes

et al. 2015

American J of Med Genetics Pt B

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Neurocognitive abilities constitute complex traits with considerable heritability. Impaired neurocognition is typically observed in schizophrenia (SZ), whereas convergent evidence has shown shared genetic determinants between neurocognition and SZ. Here, we report a genome‐wide association study (GWAS) on neuropsychological and oculomotor traits, linked to SZ, in a general population sample of healthy young males (n = 1079). Follow‐up genotyping was performed in an identically phenotyped internal sample (n = 738) and an independent cohort of young males with comparable neuropsychological measures (n = 825). Heritability estimates were determined based on genome‐wide single‐nucleotide polymorphisms (SNPs) and potential regulatory effects on gene expression were assessed in human brain. Correlations with general cognitive ability and SZ risk polygenic scores were tested utilizing meta‐analysis GWAS results by the Cognitive Genomics Consortium (COGENT) and the Psychiatric Genomics Consortium (PGC‐SZ). The GWAS results implicated biologically relevant genetic loci encoding protein targets involved in synaptic neurotransmission, although no robust individual replication was detected and thus additional validation is required. Secondary permutation‐based analysis revealed an excess of strongly associated loci among GWAS top‐ranked signals for verbal working memory (WM) and antisaccade intra‐subject reaction time variability (empirical P < 0.001), suggesting multiple true‐positive single‐SNP associations. Substantial heritability was observed for WM performance. Further, sustained attention/vigilance and WM were suggestively correlated with both COGENT and PGC‐SZ derived polygenic scores. Overall, these results imply that common genetic variation explains some of the variability in neurocognitive functioning among young adults, particularly WM, and provide supportive evidence that increased SZ genetic risk predicts neurocognitive fluctuations in the general population. © 2015 The Authors American Journal of Medical Genetics Part B: Neuropsychiatric Genetics Published by Wiley Periodicals, Inc.

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“…Haworth et al, 2010;Polderman et al, 2015;Tucker-Drob & Bates, 2016) also supports the Gene-Gini interplay. Unlike numeracy and literacy, for which heritability remains stably high throughout the school system, heritability of IQ is moderate in primary school and continues to increase throughout education (Kovas et al, 2013).…”

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confidence: 64%

Genes and Gini: What Inequality Means for Heritability

Selita

Kovas

2018

J. Biosoc. Sci.

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Summary. Research has established that genetic differences among people explain a greater or smaller proportion of the variation in life outcomes in different environmental conditions. This review evaluates the results of recent educationally relevant behavioural genetic studies and meta-analyses in the context of recent trends in income and wealth distribution. The pattern of results suggests that inequality and social policies can have profound effects on the heritability of educational attainment and achievement in a population (Gene-Gini interplay). For example, heritability is generally higher at greater equality levels, suggesting that inequality stifles the expression of educationally relevant genetic propensities. The review concludes with a discussion of the mechanisms of Gene-Gini interplay and what the findings mean for efforts to optimize education for all people.

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The heritability of general cognitive ability increases linearly from childhood to young adulthood

Cited by 546 publications

References 54 publications

Intelligence: shared genetic basis between Mendelian disorders and a polygenic trait

Intelligence: shared genetic basis between Mendelian disorders and a polygenic trait

Common genetic variation and schizophrenia polygenic risk influence neurocognitive performance in young adulthood

Genes and Gini: What Inequality Means for Heritability

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