The literature on narcissism suggests two contradictory ways how highly narcissistic individuals deal with their failures: They might avoid consciously recognising their failures to protect their ego or they might vigilantly turn towards their failures to process cues that are important for maintaining their grandiosity. We tried to dissolve these contradictory positions by studying event-related potential components of error processing and their variations with narcissism. With a speeded go/no-go task, we examined how the error-related negativity (Ne; reflecting an early, automatic processing stage) and the error positivity (Pe; associated with conscious error detection) vary with Admiration and Rivalry, two narcissism dimensions, under ego-threatening conditions. Using multilevel models, we showed that participants with high Rivalry displayed higher Ne amplitudes suggesting a heightened trait of defensive reactivity. We did not find variations of either narcissism dimension with the Pe, which would have pointed to weaker error awareness. Thus, our results only supported the second position: a heightened vigilance to errors in narcissism at early, rather automatic processing stages.

The present study examines whether self-reported trust in humans and self-reported trust in [(different) products with built-in] artificial intelligence (AI) are associated with one another and with brain structure. We sampled 90 healthy participants who provided self-reported trust in humans and AI and underwent brain structural magnetic resonance imaging assessment. We found that trust in humans, as measured by the trust facet of the personality inventory NEO-PI-R, and trust in AI products, as measured by items assessing attitudes toward AI and by a composite score based on items assessing trust toward products with in-built AI, were not significantly correlated. We also used a concomitant dimensional neuroimaging approach employing a data-driven source-based morphometry (SBM) analysis of gray-matter-density to investigate neurostructural associations with each trust domain. We found that trust in humans was negatively (and significantly) correlated with an SBM component encompassing striato-thalamic and prefrontal regions. We did not observe significant brain structural association with trust in AI. The present findings provide evidence that trust in humans and trust in AI seem to be dissociable constructs. While the personal disposition to trust in humans might be “hardwired” to the brain’s neurostructural architecture (at least from an individual differences perspective), a corresponding significant link for the disposition to trust AI was not observed. These findings represent an initial step toward elucidating how different forms of trust might be processed on the behavioral and brain level.

The aim of this study was to better understand the relation of schizotypy traits with sensory gating ability in a sample of community-dwelling individuals with high and low schizotypy traits. Sensory gating was assessed through the paired click paradigm and mid-latency evoked responses (i.e., P50, N100, P200), while schizotypy traits were assessed through the SPQ-BR which was used to classify participants into “high” and “low” schizotypy groups. Based on prior work, we hypothesized that those with the highest schizotypy scores would have reduced sensory gating ability. While this study does not show differences between relatively low and high schizotypy groups on sensory gating ability, it does suggest that our participants may have been experiencing deficits in attention allocation, a downstream cognitive processing measure. Scores on the SPQ-BR suggest that our sample was not close to the high end of the schizotypy traits which may help explain why no differences were found. This research shows the importance of including all levels of schizotypy ratings in clinical research as we can gain a clearer view of the impact of schizotypy on the brain and cognitive functioning in those with “high” levels of schizotypy. Additionally, this work highlights the importance of including measures of important factors such as impulsivity and sensation-seeking to better understand what aspects of schizotypy may be driving these sensory gating alterations reported in the literature.

The present study examines whether neuroticism is predicted by genetic vulnerability, summarized as polygenic risk score for neuroticism (PRSN), in interaction with bullying, parental bonding, and childhood adversity. Data were derived from a general population adolescent and young adult twin cohort. The final sample consisted of 202 monozygotic and 436 dizygotic twins and 319 twin pairs. The Short Eysenck Personality questionnaire was used to measure neuroticism. PRSN was trained on the results from the Genetics of Personality Consortium (GPC) and United Kingdom Biobank (UKB) cohorts, yielding two different PRSN. Multilevel mixed-effects models were used to analyze the main and interacting associations of PRSN, childhood adversity, bullying, and parental bonding style with neuroticism. We found no evidence of gene–environment correlation. PRSN thresholds of .005 and .2 were chosen, based on GPC and UKB datasets, respectively. After correction for confounders, all the individual variables were associated with the expression of neuroticism: both PRSN from GPC and UKB, childhood adversity, maternal bonding, paternal bonding, and bullying in primary school and secondary school. However, the results indicated no evidence for gene–environment interaction in this cohort. These results suggest that genetic vulnerability on the one hand and negative life events (childhood adversity and bullying) and positive life events (optimal parental bonding) on the other represent noninteracting pathways to neuroticism.

We examine some of the genetic features of neuroticism (N) taking as an animal model the Maudsley Reactive (MR) and Maudsley Nonreactive (MNR) rat strains which were selectively bred, respectively, for high and low open-field defecation (OFD) starting in the late 1950s. To draw analogies with human genetic studies, we explore the genetic correlation of N with irritable bowel syndrome (IBS). We review progress with the rat model and developments in the field of human complex trait genetics, including genetic association studies that relate to current understanding of the genetics of N. The widespread differences in the tone of the peripheral sympathetic nervous system that have been found between the Maudsley strains, particularly those observed in the colon, may underly the differences in OFD (MNR, higher sympathetic tone and zero defecation). In humans, a large genome-wide association study (GWAS) reported six genes contributing to IBS, four of which were implicated in mood and anxiety disorders or were expressed in the brain, with three of the four also expressed in the nerve fibers and ganglia of the gut. Heritability of N is estimated at around 50% in twin and family studies, and GWASs identified hundreds of loci, enabling estimation of genome-wide correlations (rg) with other traits. Significantly, the estimate for rg between risk of IBS, anxiety, N, and depression was >0.5 and suggested genetic pleiotropy without evidence for causal mechanisms. Findings on the adrenergic pharmacology of the colon, coupled with new understanding of the role of the locus ceruleus in modifying afferent information from this organ, generate hypotheses that challenge traditional cause/effect notions about the relationship of the central nervous system to peripheral events in response to stress, suggest specific targets for gene action in the Maudsley model and emphasize the value of reciprocal evaluation of genetic architecture underlying N in rodents and humans.

When looking at others, primates primarily focus on the face – detecting the face first and looking at it longer than other parts of the body. This is because primate faces, even without expression, convey trait information crucial for navigating social relationships. Recent studies on primates, including humans, have linked facial features, specifically facial width-to-height ratio (fWHR), to rank and Dominance-related personality traits, suggesting these links’ potential role in social decisions. However, studies on the association between dominance and fWHR report contradictory results in humans and variable patterns in nonhuman primates. It is also not clear whether and how nonhuman primates perceive different facial cues to personality traits and whether these may have evolved as social signals. This review summarises the variable facial-personality links, their underlying proximate and evolutionary mechanisms and their perception across primates. We emphasise the importance of employing comparative research, including various primate species and human populations, to disentangle phylogeny from socio-ecological drivers and to understand the selection pressures driving the facial-personality links in humans. Finally, we encourage researchers to move away from single facial measures and towards holistic measures and to complement perception studies using neuroscientific methods.

The Roman high-avoidance (RHA) and low-avoidance (RLA) rat lines/strains were established in Rome through bidirectional selection of Wistar rats for rapid (RHA) or extremely poor (RLA) acquisition of a two-way active avoidance task. Relative to RHAs, RLA rats exhibit enhanced threat sensitivity, anxiety, fear and vulnerability to stress, a passive coping style and increased sensitivity to frustration. Thus, RLA rats’ phenotypic profile falls well within the “internalizing” behavior spectrum. Compared with RLAs and other rat strains/stocks, RHAs present increased impulsivity and reward sensitivity, deficits in social behavior and attentional/cognitive processes, novelty-induced hyper-locomotion and vulnerability to psychostimulant sensitization and drug addiction. Thus, RHA rats’ phenotypes are consistent with a “disinhibiting externalizing” profile. Many neurobiological/molecular traits differentiate both rat lines/strains. For example, relative to RLA rats, RHAs exhibit decreased function of the prefrontal cortex (PFC), hippocampus and amygdala, increased functional tone of the mesolimbic dopamine system, a deficit of central metabotropic glutamate-2 (mGlu2) receptors, increased density of serotonin 5-HT2A receptors in the PFC, impairment of GABAergic transmission in the PFC, alterations of several synaptic markers and increased density of pyramidal immature dendrític spines in the PFC. These characteristics suggest an immature brain of RHA rats and are reminiscent of schizophrenia features like hypofrontality and disruption of the excitation/inhibition cortical balance. We review evidence supporting RLA rats as a valid model of anxiety/fear, stress and frustration vulnerability, whereas RHA rats represent a promising translational model of neurodevelopmental alterations related to impulsivity, schizophrenia-relevant features and comorbidity with drug addiction vulnerability.

While the field of personality neuroscience has extensively focused on humans and, in a few cases, primates and rodents, a wide range of research on fish personality has emerged in the last decades. This research is focused mainly on the ecological and evolutionary causes of individual differences and also aimed less extensively at proximal mechanisms (e.g., neurochemistry or genetics). We argue that, if consistent and intentional work is made to solve some of the meta-theoretical issues of personality research both on fish and mammals, fish personality research can lead to important advances in personality neuroscience as a whole. The five dimensions of personality in fish (shyness-boldness, exploration-avoidance, activity, aggressiveness, and sociability) need to be translated into models that explicitly recognize the impacts of personality in psychopathology, synergizing research on fish as model organisms in experimental psychopathology, personality neuroscience, and ecological-ethological approaches to the evolutionary underpinnings of personality to produce a powerful framework to understand individual differences.

Autism spectrum disorder (ASD) is a developmental disorder characterized by stereotypies or repetitive behaviors and impairments in social behavior and socio-communicative skills. One hallmark phenotype of ASD is poor joint attention skills compared to neurotypical controls. In addition, individuals with ASD have lower scores on several of the Big 5 personality dimensions, including Extraversion. Here, we examine these traits in a nonhuman primate model (chimpanzees; Pan troglodytes) to further understand the relationship between personality and joint attention skills, as well as the genetic and neural systems that contribute to these phenotypes. We used archival data including receptive joint attention (RJA) performance, personality based on caretaker ratings, and magnetic resonance images from 189 chimpanzees. We found that, like humans, chimpanzees who performed worse on the RJA task had lower Extraversion scores. We also found that joint attention skills and several personality dimensions, including Extraversion, were significantly heritable. There was also a borderline significant genetic correlation between RJA and Extraversion. A conjunction analysis examining gray matter volume showed that there were five main brain regions associated with both higher levels of Extraversion and social cognition. These regions included the right posterior middle and superior temporal gyrus, bilateral inferior frontal gyrus, left inferior frontal sulcus, and left superior frontal sulcus, all regions within the social brain network. Altogether, these findings provide further evidence that chimpanzees serve as an excellent model for understanding the mechanisms underlying social impairment related to ASD. Future research should further examine the relationship between social cognition, personality, genetics, and neuroanatomy and function in nonhuman primate models.