Autism is marked by substantial heterogeneity in cognitive, affective, behavioral, and neural profiles. This heterogeneity among diagnosed individuals is also reflected in the broad spread of autistic traits in the general population. Moving beyond a narrow focus on social-communication and/or repetitive-behavior differences, contemporary accounts increasingly emphasize multidimensional and transdiagnostic processes and the need to integrate evidence across levels of analysis, from self-report and cognitive measures to neuroimaging and computational models. The contributions in this Special Issue collectively advance this agenda by providing insights into individual differences in autistic traits and autism-relevant phenotypes, clarifying their measurement and stability, and proposing mechanistic frameworks that can help explain why diverse profiles emerge. In this conclusion piece, we summarize the manuscripts included in the special issue, highlight shared themes and discuss remaining issues and future directions, particularly related to naturalistic, interactive neuroscience. Ultimately, we hope this work will contribute to the development of more precise and inclusive models of autism.
Most previous studies on the link of autistic traits (ATs) to psychotic experiences (PEs) were performed in clinical populations; hence, the need for further examination of this relationship within the extended autism-and psychosis-phenotypes in the general population. This study aimed to test the following hypotheses: (1) ATs will be positively related to PEs; (2) alexithymia will act as a mediator between ATs and PEs; (3) childhood trauma will moderate the mediation model of alexithymia between ATs and PEs. This cross-sectional research took place in 12 Arab countries among 7,646 young adults. The Autism-Spectrum Quotient-28, Prodromal Questionnaire-Brief, Toronto Alexithymia Scale, and Childhood trauma Self-Report Scale-12 were used. Analysis was done using PROCESS-Macro model-7 in SPSS. Childhood abuse significantly moderated the association between ATs and alexithymia. Higher ATs were significantly associated with higher alexithymia, and this association was stronger at lower than higher levels of childhood abuse. In turn, higher alexithymia was significantly associated with higher PEs. The direct association between ATs and PEs remained significant. The conditional indirect effect of ATs on PEs through alexithymia was significant at low, moderate, and high levels of childhood abuse. Furthermore, the index of moderated mediation was significant, indicating that childhood abuse significantly moderated the indirect association between ATs and PEs through alexithymia. The current results suggest that alexithymia and childhood trauma seem to be key factors that should be considered together as specific targets for treatment to improve the severity of psychotic symptoms and even possibly prevent psychosis in highly autistic young adults.
Reinforcement sensitivity theory (RST) most clearly relates to internalizing disorders. But a weak behavioural inhibition system (BIS as defined by RST) could underlie externalising, in general, and psychopathy in particular (Fowles, 1980). Conventional “rationally derived” RST scales (rRST) are not anchored in neurally defined RST systems (nRST). So, here, we use both rRST and nRST measures to assess psychopathy traits. We operationalised psychopathy via a four-factor model (affective | interpersonal | disinhibition | boldness). We operationalised rRST via the Heym, Ferguson & Lawrence (2008) updated version of Carver and White’s (1994) BIS/BAS scales (BAS | BIS | FFFS). We operationalised nRST (goal inhibition system, GIS; goal repulsion system, GRS) via previously validated (Shadli et al., 2021) rhythmic power in the stop signal task (SST) and (goal approach system, GAS) via previously validated ERPs in the doors task. Initial bivariate correlations of psychopathy factors with rRST scales were as expected. We found no significant associations between psychopathy factors and nRST measures. A series of post hoc exploratory repeated measures ANOVAs guarded against non-linearity between psychopathy and nRST constructs. These found that: (1) Disinhibition traits might be explained (unexpectedly) by increased sensitivity in the GIS (i.e., conflict) and GRS (i.e., repulsion) and decreased sensitivity in the GAS (i.e., attraction). (2) Affective traits might be explained, as expected, by decreased sensitivity in the GIS and GRS. But an unexpected positive association was also found in the alpha frequency range for the GRS. So, nRST systems (particularly GIS) do not explain psychopathy. rRST scales were more aligned with expectations but were explained via their “rational” basis not RST per se. Unlike internalizing, nRST does not appear strongly related to externalising disorders in general and psychopathy in particular. rRST appears distinct from nRST.
In the present paper we present psychometric properties on a Social Dominance scale from items which are embedded in the Affective Neuroscience Personality Scales 3.1. In two samples we show that psychometrics of the Social Dominance scale are sufficient and that correlations with scales measuring Panksepp’s primary emotional systems fail to consistently reach statistical significance with the exception of associations with ANGER (moderate effect size), SEEKING and CARE (small effect sizes). No associations with satisfaction with life and only small negative associations with Spirituality could be observed. We concur with Panksepp that Social Dominance is not a primary emotion but is a learned secondary emotion involving several primary emotions. We show evidence that Social Dominance is not the same as ANGER. We also briefly review mammalian (including humans) evidence that supports the view that Social Dominance is learned and also that the ANGER, SEEKING, and CARE primary mammalian emotions contribute to the learning of Social Dominance.
Shame and guilt are similar yet distinct self-conscious emotions that often facilitate the attainment of social goals and motivate behaviors that promote social acceptance. Recent studies have shown that individuals with autism or high autistic traits may tend to exhibit higher shame-proneness and lower guilt-proneness. This study examined whether this profile of self-conscious emotions can be explained by the functional organization of the brain using resting-state fMRI. Autistic traits, shame- and guilt-proneness and whole-brain resting-state fMRI data were measured in 45 neurotypical individuals. Our results revealed that the positive association between autistic traits and shame-proneness was mediated by resting-state functional connectivity between the right frontal pole and several regions among the cortical midline structures, including the precuneus, anterior cingulate and posterior cingulate. Additionally, functional connectivity between the right frontal pole and precuneus was found to mediate the negative association between autistic traits and guilt-proneness. These findings highlight the role of the cortical midline structures as a key neural substrate underlying differential experiences of negative self-conscious emotions among individuals with high autistic traits.
