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Biology subjects

Mosing, M. A.

Publications and source records attributed to Mosing, M. A..

4 recordsLinked to original sources

Factors underlying creativity show distinct genetic architecture and genetic correlations with psychiatric disorders

While creativity is widely recognized as multifaceted, genome-wide association studies have largely focused on individual measures. Here, we used genomic structural equation modeling of six creativity-related GWASs and identified two latent genetic factors: a general factor and an artistic factor, with 22 and 13 genome-wide significant loci, respectively, nine of which are novel. The general factor was almost perfectly genetically correlated with educational attainment (rg = 0.96), suggesting that it primarily captured genetic influences shared with cognitive and educational processes rather than creativity-specific variation. In contrast, the artistic factor showed only a weak genetic correlation with educational attainment (rg = 0.11) and consistent positive genetic correlations with psychiatric disorders, whereas associations for the general factor were largely null or negative. Biological annotation analyses further identified distinct enrichment patterns unique to the artistic factor, providing initial evidence that different dimensions of creativity may be characterized by partially distinct neurobiological pathways.

genomics↗

Distinct genetic pathways to music enjoyment

Humans engage with music for various reasons that range from emotional regulation and relaxation to social bonding. While there are large inter-individual differences in how much humans enjoy music, little is known about the origins of those differences. Here, we disentangled the genetic factors underlying such variation. We collected behavioural data on several facets of music reward sensitivity, music perceptual ability, and general reward sensitivity from a large sample of Swedish twins (N = 9,169). We found that genetic factors substantially explain variance in music reward sensitivity above and beyond genetic influences shared with music perception and general reward sensitivity. Furthermore, multivariate analyses showed that genetic influences on the different facets of music reward sensitivity are partly distinct, uncovering distinct pathways to music enjoyment and different patterns of genetic associations with objectively assessed music perceptual abilities. These results paint a complex picture in which partially distinct sources of genetic variation contribute to different aspects of musical enjoyment and open up new possibilities for using inter-individual differences to gain insights into the biology of a key aspect of human behaviour.

genetics↗

Unravelling the genetic architecture of musical rhythm

Moving in synchrony to the beat is a fundamental component of musicality. Here, we conducted a genome-wide association study (GWAS) to identify common genetic variants associated with beat synchronization in 606,825 individuals. Beat synchronization exhibited a highly polygenic architecture, with sixty-nine loci reaching genome-wide significance (p<5x10-8) and SNP-based heritability (on the liability scale) of 13%-16%. Heritability was enriched for genes expressed in brain tissues, and for fetal and adult brain-specific gene regulatory elements, underscoring the role of central nervous system-expressed genes linked to the genetic basis of the trait. We performed validations of the self-report phenotype (through internet-based experiments) and of the GWAS (polygenic scores for beat synchronization were associated with patients algorithmically classified as musicians in medical records of a separate biobank). Genetic correlations with breathing function, motor function, processing speed, and chronotype suggest shared genetic architecture with beat synchronization and provide avenues for new phenotypic and genetic explorations.

genetics↗

Neuroticism as a predictor of frailty in old age: a genetically informative approach

ObjectiveNeuroticism is associated with poor health outcomes, but its contribution to the accumulation of health deficits in old age, i.e. frailty, is largely unknown. We aimed to explore associations between neuroticism and frailty cross-sectionally and over up to 29 years, and to investigate the contribution of shared genetic influences. MethodData were derived from the UK Biobank (UKB, n=502,631), the Australian Over 50s Study (AO50, n=3,011) and the Swedish Twin Registry (SALT n=23,744, SATSA n=1,637). Associations between neuroticism and the Frailty Index were investigated using regression analysis cross-sectionally in UKB, AO50 and SATSA, and longitudinally in SALT (25-29y follow-up) and SATSA (6 and 23y follow-up). The co-twin control method was applied to explore the contribution of underlying shared familial factors (SALT, SATSA, AO50). Genome-wide polygenic risk scores for neuroticism in all samples were used to further assess whether common genetic variants associated with neuroticism predict frailty. ResultsHigh neuroticism was consistently associated with greater frailty cross-sectionally (adjusted {beta}, 95% confidence intervals in UKB= 0.32, 0.32-0.33; AO50= 0.35, 0.31-0.39; SATSA= 0.33, 0.27-0.39) and longitudinally up to 29 years (SALT= 0.24; 0.22-0.25; SATSA 6y= 0.31, 0.24-0.38; SATSA 23y= 0.16, 0.07-0.25). When controlling for underlying shared genetic and environmental factors the neuroticism-frailty association remained significant, although decreased. Polygenic risk scores for neuroticism significantly predicted frailty in the two larger samples (meta-analyzed total {beta}= 0.06, 0.05-0.06). ConclusionHigh neuroticism is associated with the development and course of frailty. Both environmental and genetic influences, including neuroticism-associated genetic variants, contribute to this relationship.

epidemiology↗