Individual differences in music traits are heritable and correlated with the development of cognitive and communication skills, but little is known about whether diverse modes of music engagement (e.g., playing instruments vs. singing) reflect similar underlying genetic/environmental influences. Moreover, the biological etiology underlying the relationship between musicality and childhood language development is poorly understood. Here we explored genetic and environmental associations between music engagement and verbal ability in the Colorado Adoption/Twin Study of Lifespan behavioral development & cognitive aging (CATSLife). Adolescents (N = 1,684) completed measures of music engagement and intelligence at approximately age 12 and/or multiple tests of verbal ability at age 16. Structural equation models revealed that instrument engagement was highly heritable (a² = .78), with moderate heritability of singing (a² = .43) and dance engagement (a² = .66). Adolescent self-reported instrument engagement (but not singing or dance engagement) was genetically correlated with age 12 verbal intelligence and still was associated with age 16 verbal ability, even when controlling for age 12 full-scale intelligence, providing evidence for a longitudinal relationship between music engagement and language beyond shared general cognitive processes. Together, these novel findings suggest that shared genetic influences in part accounts for phenotypic associations between music engagement and language, but there may also be some (weak) direct benefits of music engagement on later language abilities. (PsycInfo Database Record (c) 2021 APA, all rights reserved).
Understanding the neuroanatomical correlates of individual differences in executive function (EF) is integral to a complete characterization of the neural systems supporting cognition. While studies have investigated EF-neuroanatomy relationships in adults, these studies often include samples with wide variation in age, which may mask relationships between neuroanatomy and EF specific to certain neurodevelopmental time points, and such studies often use unreliable single task measures of EF. Here we address both issues. First, we focused on a specific age at which the majority of neurodevelopmental changes are complete but at which age-related atrophy is not likely (N = 251; mean age of 28.71 years, SD = 0.57). Second, we assessed EF through multiple tasks, deriving three factors scores guided by the unity/diversity model of EF, which posits a common EF factor that influences all EF tasks, as well as an updating-specific and shifting-specific factor. We found that better common EF was associated with greater volume and surface area of regions in right middle frontal gyrus/frontal pole, right inferior temporal gyrus, as well as fractional anisotropy in portions of the right superior longitudinal fasciculus (rSLF) and the left anterior thalamic radiation. Better updating-specific ability was associated with greater cortical thickness of a cluster in left cuneus/precuneus, and reduced cortical thickness in regions of right superior frontal gyrus and right middle/superior temporal gyrus, but no aspects of white matter diffusion. In contrast, better shifting-specific ability was not associated with gray matter characteristics, but rather was associated with increased mean diffusivity and reduced radial diffusivity throughout much of the brain and reduced axial diffusivity in distinct clusters of the left superior longitudinal fasciculus, the corpus callosum, and the right optic radiation. These results demonstrate that associations between individual differences in EF ability and regional neuroanatomical properties occur not only within classic brain networks thought to support EF, but also in a variety of other regions and white matter tracts. These relationships appear to differ from observations made in emerging adults (Smolker et al., 2015), which might indicate that the brain systems associated with EF continue to experience behaviorally relevant maturational process beyond the early 20s.
ObjectiveTo investigate the genetic architecture of internalizing symptoms in childhood and adolescence.MethodIn 22 cohorts, multiple univariate genome-wide association studies (GWASs) were performed using repeated assessments of internalizing symptoms, in a total of 64,561 children and adolescents between 3 and 18 years of age. Results were aggregated in meta-analyses that accounted for sample overlap, first using all available data, and then using subsets of measurements grouped by rater, age, and instrument.ResultsThe meta-analysis of overall internalizing symptoms (INToverall) detected no genome-wide significant hits and showed low single nucleotide polymorphism (SNP) heritability (1.66%, 95% CI = 0.84-2.48%, neffective = 132,260). Stratified analyses indicated rater-based heterogeneity in genetic effects, with self-reported internalizing symptoms showing the highest heritability (5.63%, 95% CI = 3.08%-8.18%). The contribution of additive genetic effects on internalizing symptoms appeared to be stable over age, with overlapping estimates of SNP heritability from early childhood to adolescence. Genetic correlations were observed with adult anxiety, depression, and the well-being spectrum (|rg| > 0.70), as well as with insomnia, loneliness, attention-deficit/hyperactivity disorder, autism, and childhood aggression (range |rg| = 0.42-0.60), whereas there were no robust associations with schizophrenia, bipolar disorder, obsessive-compulsive disorder, or anorexia nervosa.ConclusionGenetic correlations indicate that childhood and adolescent internalizing symptoms share substantial genetic vulnerabilities with adult internalizing disorders and other childhood psychiatric traits, which could partially explain both the persistence of internalizing symptoms over time and the high comorbidity among childhood psychiatric traits. Reducing phenotypic heterogeneity in childhood samples will be key in paving the way to future GWAS success. To investigate the genetic architecture of internalizing symptoms in childhood and adolescence. In 22 cohorts, multiple univariate genome-wide association studies (GWASs) were performed using repeated assessments of internalizing symptoms, in a total of 64,561 children and adolescents between 3 and 18 years of age. Results were aggregated in meta-analyses that accounted for sample overlap, first using all available data, and then using subsets of measurements grouped by rater, age, and instrument. The meta-analysis of overall internalizing symptoms (INToverall) detected no genome-wide significant hits and showed low single nucleotide polymorphism (SNP) heritability (1.66%, 95% CI = 0.84-2.48%, neffective = 132,260). Stratified analyses indicated rater-based heterogeneity in genetic effects, with self-reported internalizing symptoms showing the highest heritability (5.63%, 95% CI = 3.08%-8.18%). The contribution of additive genetic effects on internalizing symptoms appeared to be stable over age, with overlapping estimates of SNP heritability from early childhood to adolescence. Genetic correlations were observed with adult anxiety, depression, and the well-being spectrum (|rg| > 0.70), as well as with insomnia, loneliness, attention-deficit/hyperactivity disorder, autism, and childhood aggression (range |rg| = 0.42-0.60), whereas there were no robust associations with schizophrenia, bipolar disorder, obsessive-compulsive disorder, or anorexia nervosa. Genetic correlations indicate that childhood and adolescent internalizing symptoms share substantial genetic vulnerabilities with adult internalizing disorders and other childhood psychiatric traits, which could partially explain both the persistence of internalizing symptoms over time and the high comorbidity among childhood psychiatric traits. Reducing phenotypic heterogeneity in childhood samples will be key in paving the way to future GWAS success.
Abstract Plagioclase crystals in plagioclase ultraphyric basalts (PUB) record changes in the major, trace, and isotopic compositions of evolving magmas. Those changes represent the record of specific processes in the crust and upper mantle that impart distinct crystal textures onto which chemical signatures are written. The extent to which the type and abundance of plagioclase textures and chemical signatures identified in one tectonic setting are found in others is still unclear. Here we report on the textural and compositional characteristics of PUB lavas from the Northeastern (NE) Pacific Ridge system (Juan de Fuca Ridge, Blanco Fracture Zone, and Gorda Ridge). The NE Pacific Ridge system exhibits a variety of populations of plagioclase megacrysts. The distribution of textural and compositional characteristics (e.g., single mode, bimodal, or trimodal distribution) are consistent with the presence of more than one parental magma in some samples. In PUB lava from the NE Pacific, we found that the populations of different textural types of plagioclase megacrysts are not compositionally distinct. Specifically, in any individual sample, there is no correlation of texture with major and trace element composition. We interpret the disconnect between texture and composition to be indicative of a system characterized by mixing of similar batches of magma resulting in populations of plagioclase megacrysts dominated by homogeneity or small degrees of normal/reverse zoning in most but not all cases. Furthermore, the populations of megacrysts and glomerocrysts are distinct in each sample and not correlated with their setting (on‐axis, off‐axis, or intra‐transform basin).
Laboratory executive function (EF) constructs, such as response inhibition, are often conceptually linked with self-report measures of impulsivity, yet their empirical correlations are low. We examined, in two twin studies ( ns = 749 and 761 individuals with EF data), the phenotypic and genetic overlap of three EF latent variables (a Common EF factor predicting response inhibition, working memory updating, and mental set-shifting tasks and Updating- and Shifting-Specific factors) with five impulsivity dimensions (negative and positive urgency, lack of premeditation and perseverance, and sensation seeking). In both samples, impulsivity dimensions were only modestly correlated phenotypically ( rs = −.20–.11) and genetically ( rAs = −.44–.04) with Common EF. In both samples, Common EF and multiple impulsivity dimensions, particularly negative urgency, independently predicted Externalizing psychopathology, and multiple impulsivity dimensions but not Common EF predicted Internalizing psychopathology. These results suggest that EFs and self-reported impulsivity tap different aspects of control that are both relevant for psychopathology.
Previous research has revealed a moderate and positive correlation between procrastination and impulsivity. However, little is known about why these two constructs are related. In the present study, we used behavior-genetics methodology to test three predictions derived from an evolutionary account that postulates that procrastination arose as a by-product of impulsivity: (a) Procrastination is heritable, (b) the two traits share considerable genetic variation, and (c) goal-management ability is an important component of this shared variation. These predictions were confirmed. First, both procrastination and impulsivity were moderately heritable (46% and 49%, respectively). Second, although the two traits were separable at the phenotypic level ( r = .65), they were not separable at the genetic level ( r genetic = 1.0). Finally, variation in goal-management ability accounted for much of this shared genetic variation. These results suggest that procrastination and impulsivity are linked primarily through genetic influences on the ability to use high-priority goals to effectively regulate actions.
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