Dataset Information

Genetic Associations Between Executive Functions and a General Factor of Psychopathology.

ABSTRACT:

Objective

Symptoms of psychopathology covary across diagnostic boundaries, and a family history of elevated symptoms for a single psychiatric disorder places an individual at heightened risk for a broad range of other psychiatric disorders. Both twin-based and genome-wide molecular methods indicate a strong genetic basis for the familial aggregation of psychiatric disease. This has led researchers to prioritize the search for highly heritable childhood risk factors for transdiagnostic psychopathology. Cognitive abilities that involve the selective control and regulation of attention, known as executive functions (EFs), are a promising set of risk factors.

Method

In a population-based sample of child and adolescent twins (n = 1,913, mean age = 13.1 years), we examined genetic overlap between both EFs and general intelligence (g) and a transdiagnostic dimension of vulnerability to psychopathology, comprising symptoms of anxiety, depression, neuroticism, aggression, conduct disorder, oppositional defiant disorder, hyperactivity, and inattention. Psychopathology symptoms in children were rated by children and their parents.

Results

Latent factors representing general EF and g were highly heritable (h² = 86%-92%), and genetic influences on both sets of cognitive abilities were robustly correlated with transdiagnostic genetic influences on psychopathology symptoms (genetic r values ranged from -0.20 to -0.38).

Conclusion

General EF and g robustly index genetic risk for transdiagnostic symptoms of psychopathology in childhood. Delineating the developmental and neurobiological mechanisms underlying observed associations between cognitive abilities and psychopathology remains a priority for ongoing research.

SUBMITTER: Harden KP

PROVIDER: S-EPMC6986791 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:BackgroundDiverse behaviour problems in childhood correlate phenotypically, suggesting a general dimension of psychopathology that has been called the p factor. The shared genetic architecture between childhood psychopathology traits also supports a genetic p. This study systematically investigates the manifestation of this common dimension across self-, parent- and teacher-rated measures in childhood and adolescence.MethodsThe sample included 7,026 twin pairs from the Twins Early Development Study (TEDS). First, we employed multivariate twin models to estimate common genetic and environmental influences on p based on diverse measures of behaviour problems rated by children, parents and teachers at ages 7, 9, 12 and 16 (depressive traits, emotional problems, peer problems, autism traits, hyperactivity, antisocial behaviour, conduct problems and psychopathic tendencies). Second, to assess the stability of genetic and environmental influences on p across time, we conducted longitudinal twin modelling of the first phenotypic principal components of childhood psychopathological measures across each of the four ages. Third, we created a genetic p factor in 7,026 unrelated genotyped individuals based on eight polygenic scores for psychiatric disorders to estimate how a general polygenic predisposition to mostly adult psychiatric disorders relates to childhood p.ResultsBehaviour problems were consistently correlated phenotypically and genetically across ages and raters. The p factor is substantially heritable (50%-60%) and manifests consistently across diverse ages and raters. However, residual variation in the common factor models indicates unique contributions as well. Genetic correlations of p components across childhood and adolescence suggest stability over time (49%-78%). A polygenic general psychopathology factor derived from studies of psychiatric disorders consistently predicted a general phenotypic p factor across development (0.3%-0.9%).ConclusionsDiverse forms of psychopathology generally load on a common p factor, which is highly heritable. There are substantial genetic influences on the stability of p across childhood. Our analyses indicate genetic overlap between general risk for psychiatric disorders in adulthood and p in childhood, even as young as age 7. The p factor has far-reaching implications for genomic research and, eventually, for diagnosis and treatment of behaviour problems.