Behavioral genetics.

Plomin, Robert; DeFries, John C.; Craig, Ian; McGuffin, Peter

doi:10.1037/10480-001

Cited by 426 publications

(600 citation statements)

References 10 publications

(10 reference 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%

“…2 In the present study, we utilize this idea to examine the effects of 43 genes implicated in autosomal recessive cognitive disorders 11 on intelligence in a Dutch sample from the general population (N = 1316; see Materials and Methods, and Supplementary Figures S1 and S2). Despite its being one of the most heritable human traits (with heritability estimates ranging from 0.6 to 0.8 in adolescence and adulthood 12,13 ), no loci consistently associated with normal-range variation in intelligence have thus far been reported. [13][14][15][16] The two largest genome-wide association studies (GWAS) to date failed to find replicable genome-wide association in SNP-based analyses in adults and children, respectively.…”

Section: Introductionmentioning

confidence: 99%

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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%

Section: Introductionmentioning

confidence: 99%

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

et al. 2015

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“…Dominance genetic effects are those due to the interaction or combination of alleles at a particular locus. Offspring receive only one allele from each parent, not a combination of two alleles (Plomin et al, 2001). For that reason dominance is not transmitted from parents and offspring and thus, there is not a D path from parents to offspring.…”

Section: Genetic Analysesmentioning

confidence: 99%

Genetic Analysis of Anger: Genetic Dominance or Competitive Sibling Interaction

Rebollo

Boomsma

2006

Behav Genet

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The knowledge of the causes and development of anger is still scarce. Previous studies on the sources of variance on Type A Behavior Pattern (TABP) related measures found variable heritability estimates ranging from 0.12 to 0.68, and large differences between MZ and DZ correlations. Some authors considered dominance genetic effects, competitive sibling interaction and sex differences as possible mechanisms to explain the results, but most studies lacked power. The present study uses a large sample of more than 2500 families, with longitudinal data from MZ and DZ pairs as well as their parents, to disentangle the sources of variance on anger. Model Fitting results showed that the sources of variance differ across sexes. For males 23% of the variance is due to additive genetic effects, and 26% to dominance genetic effects. For females 34% of the variance is due to additive genetic effects, and no dominance effects are found. There was no consistent evidence to confirm the presence of competitive sibling interaction as an alternative explanation for the low correlations in DZ males. The focus of research on the prediction of coronary heart disease (CHD) risk through psychological characteristics has recently changed from the multidimensional TABP to its emotional component: Anger. Understanding the sources of individual differences on anger can help to clarify the mechanisms that link it with CHD and its possible implications for treatment and prevention.

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“…It is rare that a speci®c cognitive trait can be explained by a single genetic variation in the population. Rather, cognitive traits typically involve complex patterns of inheritance involving many genes, each accounting for quite a tiny percentage of the behavioral variance, e.g., as little as 1 or 2% (Plomin, DeFries, McClean, & McGuf®n, 2001), in combination with environmental factors.…”

Section: Methods For Relating Genotype To Phenotypic Outcome Quantitamentioning

confidence: 99%

“…Interestingly, however, the risk is far from being 100%. Heritability ®gures based on MZ twins for autism and dyslexia are 60 and 65%, respectively (Plomin et al, 2001), suggesting that environmental factors play an important role. Noteworthy, too, is the fact that concordance rates for schizophrenia are much higher when MZ twins have shared the same placenta (Davis, Phelps, & Brancha, 1995).…”

Section: Methods For Relating Genotype To Phenotypic Outcome Quantitamentioning

confidence: 99%

Different approaches to relating genotype to phenotype in developmental disorders

Karmiloff‐Smith¹,

Scerif²,

Thomas³

2002

Developmental Psychobiology

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In this article, we discuss the complex problem of relating genotype to phenotype and challenge the simple mapping of genes to higher level cognitive modules. We examine various methods that have been used to investigate this relation including quantitative genetics, molecular genetics, animal models, and in-depth psychological and computational studies of developmental disorders. Both single gene and multiple gene disorders indicate that the relationship between genotype and phenotype is very indirect and that, rather than identifying mere snapshots of developmental outcomes, the process of ontogenetic development itself must be taken into account.

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Behavioral genetics.

Cited by 426 publications

References 10 publications

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

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

Genetic Analysis of Anger: Genetic Dominance or Competitive Sibling Interaction

Different approaches to relating genotype to phenotype in developmental disorders

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