Scientists from the Wellcome Sanger Institute (UK) studied how genetic features are linked to the mental abilities of children aged 4 to 16. It turned out that the contribution of different types of DNA variants changes with age: some associations become stronger, others weaker. The work was published in the journal Nature Human Behaviour.
The main analysis included 6,495 children of European ancestry from the Avon Longitudinal Study of Parents and Children. Data from two other British cohorts, the Millennium Cohort Study and UK Biobank, were also used. Children's IQ was measured using Wechsler tests at ages 4, 8 and 16, and school exams in English, maths and science were taken into account at ages 11 and 14. Because not all children underwent all assessments, some IQ scores were statistically reconstructed - missing values were filled in based on related data (imputation).
The authors considered two types of genetic variants. Common variants occur in more than 1% of people, and each individually makes a tiny contribution to a trait. They were combined into a polygenic score - a summary measure predicting differences in mental abilities. Rare damaging mutations disrupt gene function; to assess them, exome sequencing - reading the protein-coding regions of DNA - was used in 16,103 children and 10,140 parents.
It turned out that the association of the polygenic score linked to education and cognitive abilities with IQ strengthens with age: at age 4 it explained about 11% of IQ variation, and by age 16 already 14%. A similar trend was observed in school grades. The association of rare damaging mutations with IQ, by contrast, was strongest in early childhood and weakened by adolescence. This may explain why some adults carry mutations linked to developmental disorders but have no noticeable problems.
The strengthening of the association between the polygenic score and age was characteristic mainly of children with high IQ scores, whereas children with very low scores (the bottom 5%) did not show this trend. The negative association of rare mutations was strongest in children with low IQ at an early age, but by age 16 these differences had smoothed out.
The authors emphasise: these are statistical associations, not proof of causal mechanisms. The results are limited to a sample of Britons of European ancestry and cannot be transferred to other groups. Polygenic scores and measures of rare mutations describe trends across thousands of people and do not allow prediction of an individual child's development. The study did not include children with diagnosed developmental disorders, so conclusions about the weakening of the association of rare mutations do not apply to them.