Relative to the general population, autistic adults are at elevated risk for depression. Factors related to this risk are poorly understood, yet identifying such factors is important for improving mental health in autistic people. Emotion regulation (ER) challenges may be one such factor. However, few studies have examined ER challenges and depression in autistic adults. We examined ER challenges, depressive symptomatology and their associations in 775 (aged 18–83 years) autistic adults using network analysis, a method that permits identification of key components of ER and depression and their interrelatedness. Three non-regularized weighted undirected networks were estimated: ER challenges, depressive symptomatology, and combined ER-depressive challenges. Community structures revealed in the ER challenges and depressive symptomatology networks align with theoretical/nosological models of ER challenges/depressive symptoms as well as extant research using network analysis to examine these constructs. The combined ER challenges-depressive symptomatology network indicated that ER challenges and depressive symptomatology are interrelated but distinct constructs. These preliminary findings using cross-sectional data provide a first step in understanding associations between a candidate factor in depression vulnerability in autistic adults – ER challenges – and identify important future research directions.

Psychiatric illnesses form spectra rather than categories, with symptoms varying continuously across individuals, i.e., there is no clear break between health and disorder. Dimensional measures of behaviour and brain activity are promising targets for studying biological mechanisms that are common across disorders. Here, we assessed the extent to which neural measures of the sensitivity of the three biological systems in the reinforcement sensitivity theory (RST) could account for individual differences in a latent general factor estimated from symptom counts across externalising disorders (EXTs). RST explanatory power was pitted against reduced P300, a reliable indicator of externalising per previous research. We assessed 206 participants for DSM-5 EXTs (antisocial personality disorder, conduct disorder, attention-deficit/hyperactivity disorder, intermittent explosive disorder symptoms, alcohol use disorder, and cannabis use disorder). Of the final sample, 49% met diagnostic criteria for at least one of the EXTs. Electroencephalographic measures of the sensitivities of the behavioural activation system (BAS), the fight/flight/freeze system, and the behavioural inhibition system (BIS), as well as P300 were extracted from the gold bar-lemon and stop-signal tasks. As predicted, we found that low neural BIS sensitivity and low P300 were uniquely and negatively associated with our latent factor of externalising. Contrary to prediction, neural BAS/"dopamine" sensitivity was not associated with externalising. Our results provide empirical support for low BIS sensitivity and P300 as neural mechanisms common to disorders within the externalising spectrum; but, given the low N involved, future studies should seek to assess the replicability of our findings and, in particular, the differential involvement of the three RST systems.

Perfectionists strive for a flawless performance because they are intrinsically motivated to set and achieve high goals (personal standards perfectionism; PSP) and/or because they are afraid to be negatively evaluated by others (evaluative concern perfectionism; ECP). We investigated the differential relationships of these perfectionism dimensions with performance, post-response adaptation, error processing (reflected by two components of the event-related potential: error/correct negativity - Ne/c; error/correct positivity - Pe/c) and error detection. In contrast to previous studies, we employed a task with increased response selection complexity providing more room for perfectionistic dispositions to manifest themselves. Although ECP was related to indicators of increased preoccupation with errors, high-EC perfectionists made more errors than low-EC perfectionists. This observation may be explained by insufficient early error processing as indicated by a reduced Ne/c effect and a lack of post-response adaptation. PSP had a moderating effect on the relationship between ECP and early error processing. Our results provide evidence that pure-EC perfectionists may spend many of their cognitive resources on error-related contents and worrying, leaving less capacity for cognitive control and thus producing a structural lack of error processing.

Recently developed quantitative models of psychopathology (i.e., Hierarchical Taxonomy of Psychopathology) identify an Antagonistic Externalizing spectrum that captures the psychological disposition toward criminal and antisocial behavior. The purpose of the present study was to examine relations between Antagonistic psychopathology (and associated Five-Factor model Antagonism/Agreeableness) and neural functioning related to social-cognitive Theory of Mind using a large sample (N = 973) collected as part of the Human Connectome Project (Van Essen et al., 2013a). No meaningful relations between Antagonism/Antagonistic Externalizing and Theory of Mind-related neural activity or synchrony were observed (p < .005). We conclude by outlining methodological considerations (e.g., validity of social cognition task and low test-retest reliability of functional biomarkers) that may account for these null results, and present recommendations for future research.

Regulatory focus theory (RFT) postulates two cognitive-motivational systems for personal goal pursuit: the promotion system, which is associated with ideal goals (an individual's hopes, dreams, and aspirations), and the prevention system, which is associated with ought goals (an individual's duties, responsibilities, and obligations). The two systems have been studied extensively in behavioral research with reference to differences between promotion and prevention goal pursuit as well as the consequences of perceived attainment versus nonattainment within each system. However, no study has examined the neural correlates of each combination of goal domain and goal attainment status. We used a rapid masked idiographic goal priming paradigm and functional magnetic resonance imaging to present individually selected promotion and prevention goals, which participants had reported previously that they were close to attaining ("match") or far from attaining ("mismatch"). Across the four priming conditions, significant activations were observed in bilateral insula (Brodmann area (BA) 13) and visual association cortex (BA 18/19). Promotion priming discriminantly engaged left prefrontal cortex (BA 9), whereas prevention priming discriminantly engaged right prefrontal cortex (BA 8/9). Activation in response to promotion goal priming was also correlated with an individual difference measure of perceived success in promotion goal attainment. Our findings extend the construct validity of RFT by showing that the two systems postulated by RFT, under conditions of both attainment and nonattainment, have shared and distinct neural correlates that interface logically with established network models of self-regulatory cognition.

Theories in personality neuroscience must aim to be consistent with several levels of explanation. If we view personality traits as constructs located only at the psychological level, we must still make their explanations compatible with observations and theories at lower levels, particularly with what we know at the neural level. If we view personality traits as constructs located only at the neural level, we will still need to predict their emergent effects at the psychological level. Personality theory at present treats traits as psychological-level constructs, with even the recent neurally oriented Cybernetic Big Five Theory specified in terms of a "conceptual nervous system" and not requiring complete or immediate translation into neural mechanisms. Here, we argue for the existence of phylogenetically old, neural-level traits that are substantially conserved across many vertebrate species. We first ask what known mechanisms control trait-like properties of neural systems: Focusing on hormones, the GABAA receptor, and amine neurotransmitter systems. We derive from what we know about these sources of neuronal modulation some metatheoretical principles to guide the future development of those aspects of personality theory, starting with neural-level trait constructs and drawing implications for higher-level trait psychology observations. Current descriptive approaches such as the Big Five are an essential precursor to personality neuroscience, but may not map one-to-one to the mechanisms and constructs of a neuroscience-based approach to traits.

Metacognition is the capacity to evaluate and control one’s own cognitive processes. Metacognition operates over a range of cognitive domains, such as perception and memory, but the neurocognitive architecture supporting this ability remains controversial. Is metacognition enabled by a common, domain-general resource that is recruited to evaluate performance on a variety of tasks? Or is metacognition reliant on domain-specific modules? This article reviews recent literature on the domain-generality of human metacognition, drawing on evidence from individual differences and neuroimaging. A meta-analysis of behavioral studies found that perceptual metacognitive ability was correlated across different sensory modalities, but found no correlation between metacognition of perception and memory. However, evidence for domain-generality from behavioral data may suffer from a lack of power to identify correlations across model parameters indexing metacognitive efficiency. Neuroimaging data provide a complementary perspective on the domain-generality of metacognition, revealing co-existence of neural signatures that are common and distinct across tasks. We suggest that such an architecture may be appropriate for “tagging” generic feelings of confidence with domain-specific information, in turn forming the basis for priors about self-ability and modulation of higher-order behavioral control.

A converging literature has revealed the existence of a set of largely consistent, hierarchically organized personality traits, that is broader traits are able to be differentiated into more fine-grained traits, in both humans and chimpanzees. Despite recent work suggesting a neural basis to personality in chimpanzees, little is known with regard to the involvement of limbic structures (i.e., amygdala and hippocampus), which are thought to play important roles in emotion. Using saved maximum likelihood estimated exploratory factor scores (two to five factors) in the context of a series of path analyses, the current study examined associations among personality dimensions across various levels of the personality hierarchy and individual variability of amygdala and hippocampal grey matter (GM) volume in a sample of captive chimpanzees (N=191). Whereas results revealed no association between personality dimensions and amygdala volume, a more nuanced series of associations emerged between hippocampal GM volume and personality dimensions at various levels of the hierarchy. Hippocampal GM volume associated most notably with Alpha (a dimension reflecting a tendency to behave in an undercontrolled and agonistic way) at the most basic two-factor level of the hierarchy; associated positively with Disinhibition at the next level of the hierarchy ("Big Three"); and finally, associated positively with Impulsivity at the most fine-grained level ("five-factor model") of the hierarchy. Findings underscore the importance of the hippocampus in the neurobiological foundation of personality, with support for its regulatory role of emotion. Further, results suggest the importance of the distinction between structure and function, particularly with regard to the amygdala.

Personality and individual differences originate from the brain. Despite major advances in the affective and cognitive neurosciences, however, it is still not well understood how personality and single personality traits are represented within the brain. Most research on brain-personality correlates has focused either on morphological aspects of the brain such as increases or decreases in local gray matter volume, or has investigated how personality traits can account for individual differences in activation differences in various tasks. Here, we propose that personality neuroscience can be advanced by adding a network perspective on brain structure and function, an endeavor that we label personality network neuroscience. With the rise of resting-state functional magnetic resonance imaging (MRI), the establishment of connectomics as a theoretical framework for structural and functional connectivity modeling, and recent advancements in the application of mathematical graph theory to brain connectivity data, several new tools and techniques are readily available to be applied in personality neuroscience. The present contribution introduces these concepts, reviews recent progress in their application to the study of individual differences, and explores their potential to advance our understanding of the neural implementation of personality. Trait theorists have long argued that personality traits are biophysical entities that are not mere abstractions of and metaphors for human behavior. Traits are thought to actually exist in the brain, presumably in the form of conceptual nervous systems. A conceptual nervous system refers to the attempt to describe parts of the central nervous system in functional terms with relevance to psychology and behavior. We contend that personality network neuroscience can characterize these conceptual nervous systems on a functional and anatomical level and has the potential do link dispositional neural correlates to actual behavior.