Genetics, genes, genomics and g

Plomin, Robert

doi:10.1038/sj.mp.4001249

Cited by 34 publications

(39 citation statements)

References 57 publications

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“…Our study is in agreement with previous studies in children showing that variance in IQ test performance is for 25 to 70% accounted for by genetic variation between individuals (Bartels, Rietveld, Van Baal, & Boomsma, 2002;Hoekstra, Bartels, & Boomsma, 2007;Jacobs et al, 2001;Plomin, 2003;Rietveld, Dolan, Van Baal, & Boomsma, 2003;Turkheimer, Haley, Waldron, D'Onofrio, & Gottesman, 2003). Genetic factors entirely explain the significant phenotypic correlations between the three brain volumes and IQ, PO and PS.…”

Section: Discussionsupporting

confidence: 82%

A genetic analysis of brain volumes and IQ in children

et al. 2009

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Section: Discussionsupporting

confidence: 82%

A genetic analysis of brain volumes and IQ in children

et al. 2009

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“…Indeed, heritability estimates for cognitive ability, or 'g', are reported to increase with age (e.g. see Plomin, 2003). An alternative explanation of the restriction of the significant findings to the older groups could be that the limiting effect of FMR1 allele length on cognitive ability may only develop with age.…”

Section: Discussionmentioning

confidence: 99%

“…Similarly, English language ability was measured by teachers' assessments on UK National Curriculum (NC) Key Stage 1 criteria for English attainment (QCA Key Stage 1 Handbook, 1999, 2003. The assessments were obtained by postal questionnaire during the spring semester.…”

Section: English Atmentioning

confidence: 99%

Investigating the Relationship Between FMR1 Allele Length and Cognitive Ability in Children: A Subtle Effect of the Normal Allele Range on the Normal Ability Range?

Loat¹,

Craig²,

Plomin³

et al. 2006

Annals of Human Genetics

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SummaryThe FMR1 gene contains a trinucleotide repeat tract which can expand from a normal size of around 30 repeats to over 200 repeats, causing mental retardation (Fragile X Syndrome). Evidence suggests that premutation males (55-200 repeats) are susceptible to a late-onset tremor/ataxia syndrome and females to premature ovarian failure, and that intermediate alleles (∼ 41-55 repeats) and premutations may be in excess in samples with special educational needs. We explored the relationship between FMR1 allele length and cognitive ability in 621 low ability and control children assessed at 4 and 7 years, as well as 122 students with high IQ. The low and high ability and control samples showed no between-group differences in incidence of longer alleles. In males there was a significant negative correlation between allele length and non-verbal ability at 4 years (p = 0.048), academic achievement in maths (p = 0.003) and English (p = 0.011) at 7 years, and IQ in the high ability group (p = 0.018). There was a significant negative correlation between allele length and a standardised score for IQ and general cognitive ability at age 7 in the entire male sample (p = 0.002). This suggests that, within the normal spectrum of allele length, increased repeat numbers may have a limiting influence on cognitive performance.

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“…1 This implies that genes associated with one cognitive ability are highly likely to be associated with other cognitive abilities. These quantitative genetic findings make general intelligence an excellent target for molecular genetic research, as indicated in a recent special section of this journal, 2 which included a report of a direct association between normal variation in intelligence and a functional polymorphism in the Cathepsin D (CTSD) gene, 3 and a report of an indirect association (that is, based on linkage disequilibrium) with a polymorphism in the cholinergic muscarinic 2 receptor gene that has not yet been shown to be functional. 4 These papers add to other recent reports of direct associations between cognitive abilities and functional polymorphisms in the catechol O-methyltransferase (COMT) gene 5,6 and the brain-derived neurotrophic factor gene.…”

Section: Introductionmentioning

confidence: 99%

A functional polymorphism in the succinate-semialdehyde dehydrogenase (aldehyde dehydrogenase 5 family, member A1) gene is associated with cognitive ability

et al. 2004

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Succinate-semialdehyde dehydrogenase (SSADH) deficiency is a rare cause of learning disability. We have investigated SSADH to assess its contribution to cognitive ability in the general population in both case-control-and family-based analyses. Sequence analysis of SSADH revealed four changes affecting the encoded protein, only one of which had a minor allele whose frequency is even moderately common. We genotyped this functional polymorphism in 197 high-IQ cases, 201 average-IQ controls and 196 parent high-IQ offspring trios. The minor allele was significantly less frequent in high-IQ cases and was significantly less frequently transmitted by parents to high-IQ subjects than chance expectation. A previous study has shown that the minor allele encodes a lower activity enzyme than the major allele. These data suggest that higher SSADH activity is associated with higher intelligence across the general population. The effect is small, with each allele having an effect size translating to about 1.5 IQ points.

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Genetics, genes, genomics and g

Cited by 34 publications

References 57 publications

A genetic analysis of brain volumes and IQ in children

A genetic analysis of brain volumes and IQ in children

Investigating the Relationship Between FMR1 Allele Length and Cognitive Ability in Children: A Subtle Effect of the Normal Allele Range on the Normal Ability Range?

A functional polymorphism in the succinate-semialdehyde dehydrogenase (aldehyde dehydrogenase 5 family, member A1) gene is associated with cognitive ability

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