Genetic influence on cognitive development between childhood and adulthood

Mollon, Josephine; Knowles, Emma; Mathias, Samuel R.; Gur, Ruben C.; Peralta, Juan M.; Weiner, Daniel J.; Robinson, Elise; Gur, Raquel E.; Blangero, John; Almasy, Laura; Glahn, David C.

doi:10.1038/s41380-018-0277-0

Cited by 37 publications

(58 citation statements)

References 65 publications

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“…The vector of g loadings is the g loadings for the 10 subtests found to be MI for African and European-Americans. The vector of heritability is the average of the African-and European-American heritabilities reported by Mollon et al [65]. The vectors of group differences were: (1) the correlation with European ancestry (for the combined sample), (2) the correlation with MTAG 10K eduPGS for the European-American sample, (3) the correlation with MTAG 10k eduPGS for the monoracial African-American sample, and (4) the African-/European-American mean group differences.…”

Section: The Spearman-jensen Hypothesismentioning

confidence: 99%

Global Ancestry and Cognitive Ability

Lasker

Pesta

Fuerst

et al. 2019

Psych

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Using data from the Philadelphia Neurodevelopmental Cohort, we examined whether European ancestry predicted cognitive ability over and above both parental socioeconomic status (SES) and measures of eye, hair, and skin color. First, using multi-group confirmatory factor analysis, we verified that strict factorial invariance held between self-identified African and European-Americans. The differences between these groups, which were equivalent to 14.72 IQ points, were primarily (75.59%) due to difference in general cognitive ability (g), consistent with Spearman's hypothesis. We found a relationship between European admixture and g. This relationship existed in samples of (a) self-identified monoracial African-Americans (B = 0.78, n = 2,179), (b) monoracial African and biracial African-European-Americans, with controls added for self-identified biracial status (B = 0.85, n = 2407), and (c) combined European, African-European, and African-American participants, with controls for self-identified race/ethnicity (B = 0.75, N = 7,273). Controlling for parental SES modestly attenuated these relationships whereas controlling for measures of skin, hair, and eye color did not. Next, we validated four sets of polygenic scores for educational attainment (eduPGS). MTAG, the multi-trait analysis of genome-wide association study (GWAS) eduPGS (based on 8442 overlapping variants) predicted g in both the monoracial African-American (r = 0.111, n = 2179, p < 0.001), and the European-American (r = 0.227, n = 4914, p < 0.001) subsamples. We also found large race differences for the means of eduPGS (d = 1.89). Using the ancestry-adjusted association between MTAG eduPGS and g from the monoracial African-American sample as an estimate of the transracially unbiased validity of eduPGS (B = 0.124), the results suggest that as much as 20%-25% of the race difference in g can be naïvely explained by known cognitive ability-related variants. Moreover, path analysis showed that the eduPGS substantially mediated associations between cognitive ability and European ancestry in the African-American sample. Subtest differences, together with the effects of both ancestry and eduPGS, had near-identity with subtest g-loadings. This finding confirmed a Jensen effect acting on ancestry-related differences. Finally, we confirmed measurement invariance along the full range of European ancestry in the combined sample using local structural equation modeling. Results converge on genetics as a potential partial explanation for group mean differences in intelligence.Psych 2019, 1 433 between ancestry and outcomes or that ancestry is a non-causal correlate of the trait in question that's actually caused by something else if the mediation is not spurious. Ultimately, controls alone cannot establish causality [50].Four studies we know of have related genetically-assessed ancestry to cognitive ability in samples of 25,51,52]. Others have done this for Hispanic Americans [24,25] and various groups in Latin America [53][54][55]. Of these, the earlier ones [51-54] re...

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Section: The Spearman-jensen Hypothesismentioning

confidence: 99%

Global Ancestry and Cognitive Ability

Lasker

Pesta

Fuerst

et al. 2019

Psych

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“…The battery also included the reading subtest of the Wide Range Achievement Test (WRAT), a measure of general verbal knowledge. As in our prior work [23], we derived a general composite score (g) as the first component of principal component analysis (PCA) of accuracy scores. We also derived a general composite score for speed (gs) as the first component of PCA of reaction times.…”

Section: Cognitive Assessmentmentioning

confidence: 99%

“…Early life psychopathology is also underpinned by genes, with evidence of substantial genetic effects on childhood and adolescent psychopathology [9,10], as well as specific psychotic [11,12], externalizing [13][14][15], internalizing [16], and anxiety/depression symptoms [17][18][19][20][21]. Since cognition in early life is also influenced by genes [22,23], recent studies have examined whether there is a genetic component to cognitive correlates of early life psychopathology. Evidence from twin and family studies shows genetic overlap between psychopathology and cognitive ability [24], psychopathology and executive functions [25], ADHD and IQ [26], ADHD and executive functions [27,28], and inattention and attention regulation [29].…”

Section: Introductionmentioning

confidence: 99%

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Genetic influences on externalizing psychopathology overlap with cognitive functioning and show developmental variation

et al. 2021

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Background Questions remain regarding whether genetic influences on early life psychopathology overlap with cognition and show developmental variation. Methods Using data from 9,421 individuals aged 8 to 21 from the Philadelphia Neurodevelopmental Cohort, factors of psychopathology were generated using a bifactor model of item-level data from a psychiatric interview. Five orthogonal factors were generated: anxious-misery (mood and anxiety), externalizing (attention deficit hyperactivity and conduct disorder), fear (phobias), psychosis-spectrum, and a general factor. Genetic analyses were conducted on a subsample of 4,662 individuals of European American ancestry. A genetic relatedness matrix was used to estimate heritability of these factors, and genetic correlations with executive function, episodic memory, complex reasoning, social cognition, motor speed, and general cognitive ability. Gene × Age analyses determined whether genetic influences on these factors show developmental variation. ResultsExternalizing was heritable (h 2 =0.46, p=1x10 -6 ), but not anxious-misery (h 2 =0.09, p=0.183), fear (h 2 =0.04, p=0.337), psychosis-spectrum (h 2 =0.00, p=0.494) or general psychopathology (h 2 =0.21, p=0.040). Externalizing showed genetic overlap with face memory (ρ g =-0.412, p=0.004), verbal reasoning (ρ g =-0.485, p=0.001), spatial reasoning (ρ g =-0.426, p=0.010), motor speed (ρ g =0.659, p=1x10 -4 ), verbal knowledge (ρ g =-0.314, p=0.002), and general cognitive ability (g)(ρ g =-0.394, p=0.002). Gene × Age analyses revealed decreasing genetic variance (γ g = -0.146, p = 0.004), and increasing environmental variance (γ e = 0.059, p = 0.009) on externalizing.Conclusions Cognitive impairment may be a useful endophenotype of externalizing psychopathology and, therefore, help elucidate its pathophysiological underpinnings. Decreasing genetic variance suggests that gene discovery efforts may be more fruitful in children than adolescents or young adults.

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“…Alternatively, different environmental factors in childhood may reduce the effect of exposure to abnormal glucose tolerance levels in utero 50 . Another possible explanation is based on the heritability of cognitive development including attention and memory 51,52 . Studies showed that the heritability of cognition depended on the developmental period (it increases from around 40% in early childhood to over 80% in elders), reflecting increasing active gene‐environment correlation as positive feedback loops (eg brighter children seek more cognitive stimulation) 53 .…”

Section: Commentmentioning

confidence: 99%

Maternal glucose tolerance in pregnancy and child cognitive and behavioural problems in early and mid‐childhood

Faleschini

Rifas‐Shiman

et al. 2020

Paediatric Perinatal Epid

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Background Maternal abnormal glucose tolerance during pregnancy may adversely affect offspring cognition and behaviour, but few prospective studies investigated this association at multiple points throughout childhood. Objectives We hypothesised that maternal abnormal glucose tolerance is associated with child cognitive and behavioural outcomes in early and mid‐childhood. Methods We examined the associations of maternal abnormal glucose tolerance at 26‐28 weeks of pregnancy with offspring cognitive and behavioural scores in 1421 children in the Project Viva pre‐birth cohort. In early (mean 3.3 years) and mid‐childhood (mean 7.9 years), we measured child cognition using validated instruments, the Kaufman Brief Intelligence Test, Wide Range Assessment of Memory and Learning, and the Wide Range Assessment of Visual Motor Abilities (WRAVMA); we assessed parent‐ and teacher‐rated behavioural outcomes with the Strengths and Difficulties Questionnaire and the Behavioural Rating Inventory of Executive Function. We used linear regression models adjusted for potential confounders (maternal race/ethnicity, pre‐pregnancy BMI, intelligence, age, parity, smoking status, education, and household income at enrolment, in addition to child's sex and age at assessment). Results Of 1421 mothers, 69 (4.9%) had gestational diabetes mellitus, 43 (3.0%) impaired glucose tolerance, 122 (8.6%) isolated hyperglycaemia, and 1187 (83.5%) normal glucose tolerance. Offspring born to women with gestational diabetes mellitus had lower total WRAVMA scores (−3.09 points; 95% CI −6.12, −0.05) in early childhood compared with offspring of women with normal glucose tolerance. None of the abnormal glucose tolerance categories during pregnancy were associated with any of the cognitive outcomes (verbal, non‐verbal, and visual motor scores) or behavioural measures in mid‐childhood. Conclusions Children born to mothers who had gestational diabetes mellitus had slightly lower scores on one cognitive test in early childhood. We found no evidence to support that maternal abnormal glucose tolerance was associated with cognitive or behavioural development in mid‐childhood.

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Genetic influence on cognitive development between childhood and adulthood

Cited by 37 publications

References 65 publications

Global Ancestry and Cognitive Ability

Global Ancestry and Cognitive Ability

Genetic influences on externalizing psychopathology overlap with cognitive functioning and show developmental variation

Maternal glucose tolerance in pregnancy and child cognitive and behavioural problems in early and mid‐childhood

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