Heritable influences on amygdala and orbitofrontal cortex contribute to genetic variation in core dimensions of personality.

While many studies have reported that individual differences in personality traits are genetically influenced, the neurobiological bases mediating these influences have not yet been well characterized. To advance understanding concerning the pathway from genetic variation to personality, here we examined whether measures of heritable variation in neuroanatomical size in candidate regions (amygdala and medial orbitofrontal cortex) were associated with heritable effects on personality. A sample of 486 middle-aged (mean=55 years) male twins (complete MZ pairs=120; complete DZ pairs=84) underwent structural brain scans and also completed measures of two core domains of personality: positive and negative emotionality. After adjusting for estimated intracranial volume, significant phenotypic (r(p)) and genetic (r(g)) correlations were observed between left amygdala volume and positive emotionality (r(p)=.16, p<.01; r(g)=.23, p<.05, respectively). In addition, after adjusting for mean cortical thickness, genetic and nonshared-environmental correlations (r(e)) between left medial orbitofrontal cortex thickness and negative emotionality were also observed (r(g)=.34, p<.01; r(e)=-.19, p<.05, respectively). These findings support a model positing that heritable bases of personality are, at least in part, mediated through individual differences in the size of brain structures, although further work is still required to confirm this causal interpretation

Heritable influences on amygdala and orbitofrontal cortex contribute to genetic variation in core dimensions of personality

While many studies have reported that individual differences in personality traits are genetically influenced, the neurobiological bases mediating these influences have not yet been well characterized. To advance understanding concerning the pathway from genetic variation to personality, here we examined whether measures of heritable variation in neuroanatomical size in candidate regions (amygdala and medial orbitofrontal cortex) were associated with heritable effects on personality. A sample of 486 middle-aged (mean = 55 years) male twins (complete MZ pairs = 120; complete DZ pairs = 84) underwent structural brain scans and also completed measures of two core domains of personality: positive and negative emotionality. After adjusting for estimated intracranial volume, significant phenotypic (r(p)) and genetic (r(g)) correlations were observed between left amygdala volume and positive emotionality (r(p) = .16, p < .01; r(g) = .23, p < .05, respectively). In addition, after adjusting for mean cortical thickness, genetic and nonshared-environmental correlations (r(e)) between left medial orbitofrontal cortex thickness and negative emotionality were also observed (r(g) = .34, p < .01; r(e) = −.19, p < .05, respectively). These findings support a model positing that heritable bases of personality are, at least in part, mediated through individual differences in the size of brain structures, although further work is still required to confirm this causal interpretation

Neuroanatomical Correlates of Bifactor Model of Internalizing Psychopathology Across The Lifespan

High rates of comorbidity between internalizing disorders and heterogeneity in the behavioral manifestations of a single disorder have made it challenging to identify biological signatures of specific mental illnesses. This may in part be due to the case-control frameworks which dominate psychopathology research, frameworks which draw stark distinctions between patients and healthy individuals despite evidence that such distinctions may not reflect the distribution of behavior across the population. To address these issues, there has been a recent emphasis on employing dimensional models of psychopathology which characterize psychopathology as arising through the interaction of behaviors that are continuously distributed throughout the general population. In the current dissertation project, we first propose a novel six-factor dimensional model of internalizing psychopathology and demonstrate that dimensions in this model show preferential associations with specific internalizing disorders. We then employ gray matter morphometry analyses to identify the degree to which individual differences in internalizing dimensions are associated with structural properties of gray matter across the brain. Finally, we evaluate which dimensions are driven by genes or the environment, as well as the degree to which relationships between these dimensions and gray matter structure result from overlapping genetic or environmental influences. Our findings suggest 1) previous dimensional models of internalizing psychopathology may be improved by including cognitive dimensions of behavior, including rumination and repetitive negative thought, 2) the brain regions associated with internalizing dimensions are more distributed than the regions identified in case-control studies while also changing with age and differing by sex, and 3) behaviors that are common across internalizing disorders are largely genetic in nature, whereas behaviors that are specific to anxiety may be influenced by shared environmental factors.</p

Social reward and threat processing

The aim of this project was to investigate the relationships between individual differences in social expectancies and motivation, and how these relate to broader personality traits and to social integration outcomes such as individuals’ sense of belonging. A cognitive model of social motivation and reactivity to social feedback was proposed. In this model, generalised expectancies are considered to play a pivotal role in motivating human social behaviour. Two novel measures were developed: the levels of dispositional expectancies of social threat and reward scale (the LODESTARS) and a task-based measure of social motivation and reactivity to social reward and punishment (the social and monetary incentive delay (SMID) task). Rigorous validation studies were employed to ensure the validity and utility of these measures. The research reported in this thesis employed multiple methods: self-report, task-based measures, and structural and functional (blood oxygenation-level-dependent; BOLD) neuroimaging. The findings of all studies conducted supported the key proposal that dispositional biases in expectancies of social reward and punishment are critical for understanding individual differences in reactivity to social feedback and social outcomes such as loneliness. In the proposed model, expectancies exert their effects both by informing social approach and avoidance motivations and by directly influencing perceptions of and reactions to social cues. Convergent findings from the multiple modalities employed were consistent with both these proposed mechanisms