scholarly journals Meta-Analysis of Genetic Variation in DTNBP1 and General Cognitive Ability

2010 ◽  
Vol 68 (12) ◽  
pp. 1126-1133 ◽  
Author(s):  
Jian-Ping Zhang ◽  
Katherine E. Burdick ◽  
Todd Lencz ◽  
Anil K. Malhotra
Author(s):  
Frances M. Nilsen ◽  
Jazmin D.C. Ruiz ◽  
Nicolle S. Tulve

General cognitive ability, often referred to as ‘general intelligence’, comprises a variety of correlated abilities. Childhood general cognitive ability is a well-studied area of research and can be used to predict social outcomes and perceived success. Early life stage (e.g., prenatal, postnatal, toddler) exposures to stressors (i.e., chemical and non-chemical stressors from the total (built, natural, social) environment) can impact the development of childhood cognitive ability. Building from our systematic scoping review (Ruiz et al., 2016), we conducted a meta-analysis to evaluate more than 100 stressors related to cognitive development. Our meta-analysis identified 23 stressors with a significant increase in their likelihood to influence childhood cognitive ability by 10% or more, and 80 stressors were observed to have a statistically significant effect on cognitive ability. Stressors most impactful to cognition during the prenatal period were related to maternal health and the mother’s ability to access information relevant to a healthy pregnancy (e.g., diet, lifestyle). Stressors most impactful to cognition during the early childhood period were dietary nutrients (infancy), quality of social interaction (toddler), and exposure to toxic substances (throughout early childhood). In conducting this analysis, we examined the relative impact of real-world exposures on cognitive development to attempt to understand the inter-relationships between exposures to both chemical and non-chemical stressors and early developmental life stages. Our findings suggest that the stressors observed to be the most influential to childhood cognitive ability are not permanent and can be broadly categorized as activities/behaviors which can be modified to improve childhood cognition. This meta-analysis supports the idea that there are complex relationships between a child’s total environment and early cognitive development.


2014 ◽  
Vol 281 (1781) ◽  
pp. 20140117 ◽  
Author(s):  
Riccardo E. Marioni ◽  
Lars Penke ◽  
Gail Davies ◽  
Jennifer E. Huffman ◽  
Caroline Hayward ◽  
...  

Human cognitive ability shows consistent, positive associations with fitness components across the life-course. Underlying genetic variation should therefore be depleted by selection, which is not observed. Genetic variation in general cognitive ability (intelligence) could be maintained by a mutation–selection balance, with rare variants contributing to its genetic architecture. This study examines the association between the total number of rare stop-gain/loss, splice and missense exonic variants and cognitive ability in childhood and old age in the same individuals. Exome array data were obtained in the Lothian Birth Cohorts of 1921 and 1936 (combined N = 1596). General cognitive ability was assessed at age 11 years and in late life (79 and 70 years, respectively) and was modelled against the total number of stop-gain/loss, splice, and missense exonic variants, with minor allele frequency less than or equal to 0.01, using linear regression adjusted for age and sex. In both cohorts and in both the childhood and late-life models, there were no significant associations between rare variant burden in the exome and cognitive ability that survived correction for multiple testing. Contrary to our a priori hypothesis, we observed no evidence for an association between the total number of rare exonic variants and either childhood cognitive ability or late-life cognitive ability.


2015 ◽  
Vol 27 (9) ◽  
pp. 1766-1774 ◽  
Author(s):  
Matthew A. Scult ◽  
Joey W. Trampush ◽  
Fengyu Zheng ◽  
Emily Drabant Conley ◽  
Todd Lencz ◽  
...  

Here we provide novel convergent evidence across three independent cohorts of healthy adults (n = 531), demonstrating that a common polymorphism in the gene encoding the α2 subunit of neuronal voltage-gated type II sodium channels (SCN2A) predicts human general cognitive ability or “g.” Using meta-analysis, we demonstrate that the minor T allele of a common polymorphism (rs10174400) in SCN2A is associated with significantly higher “g” independent of gender and age. We further demonstrate using resting-state fMRI data from our discovery cohort (n = 236) that this genetic advantage may be mediated by increased capacity for information processing between the dorsolateral PFC and dorsal ACC, which support higher cognitive functions. Collectively, these findings fill a gap in our understanding of the genetics of general cognitive ability and highlight a specific neural mechanism through which a common polymorphism shapes interindividual variation in “g.”


2021 ◽  
Vol 87 ◽  
pp. 102430
Author(s):  
María Vélez-Coto ◽  
Sandra Rute-Pérez ◽  
Miguel Pérez-García ◽  
Alfonso Caracuel

2006 ◽  
Vol 15 (10) ◽  
pp. 1563-1568 ◽  
Author(s):  
Katherine E. Burdick ◽  
Todd Lencz ◽  
Birgit Funke ◽  
Christine T. Finn ◽  
Philip R. Szeszko ◽  
...  

2010 ◽  
Vol 167 (4) ◽  
pp. 436-443 ◽  
Author(s):  
Katherine E. Burdick ◽  
Pamela DeRosse ◽  
John M. Kane ◽  
Todd Lencz ◽  
Anil K. Malhotra

2007 ◽  
Vol 28 (3) ◽  
pp. 161-164 ◽  
Author(s):  
Rosalind Arden ◽  
Nicole Harlaar ◽  
Robert Plomin

Abstract. An association between intelligence at age 7 and a set of five single-nucleotide polymorphisms (SNPs) has been identified and replicated. We used this composite SNP set to investigate whether the associations differ between boys and girls for general cognitive ability at ages 2, 3, 4, 7, 9, and 10 years. In a longitudinal community sample of British twins aged 2-10 (n > 4,000 individuals), we found that the SNP set is more strongly associated with intelligence in males than in females at ages 7, 9, and 10 and the difference is significant at 10. If this finding replicates in other studies, these results will constitute the first evidence of the same autosomal genes acting differently on intelligence in the two sexes.


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