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The current study used a multifaceted approach to assess whether children with ASD have a distinctive diurnal rhythm of cortisol that differentiates them from typically developing (TD) peers and whether sub-groups of ASD children can be identified with unique diurnal profiles. Salivary cortisol was sampled at four time points during the day (waking, 30-min post-waking, afternoon, and evening) across three days in a sample of 36 children with autism spectrum disorder (ASD) and 27 typically developing (TD) peers. Between-group comparisons on both mean levels and featural components of diurnal cortisol indicated elevated evening cortisol and a dampened linear decline across the day in the ASD group. No differences were evident on the cortisol awakening response (CAR). Group-based trajectory modeling indicated that a subgroup (25%) of ASD children demonstrated an attenuated linear decline while the cortisol trajectory of the second subgroup was indistinguishable from that of the TD group. Intraclass correlations indicated that, when aggregated across days, cortisol measures were generally stable over the interval assessed. There were few significant relations between cortisol measures or sub-groups and measures of stress, temperament, and symptoms. Results encourage follow-up studies to investigate the functional significance, heterogeneity and longer-term stability of diurnal cortisol profiles in children with ASD.

Individuals with autism spectrum disorder (ASD) report high levels of co-occurring mood disorders. Previous work suggests that people with ASD also experience aberrant responses to social reward compared to typically developing (TD) peers. In the TD population, aberrant reward processing has been linked to anhedonia (i.e., loss of pleasure), which is a hallmark feature of depression. This study examined the interplay between self-reported pleasure from social and non-social rewards, autism symptom severity, loneliness, and depressive symptoms across adults with autism spectrum disorder (ASD; N=49), TD currently depressed adults (TD-dep; N=30), and TD never depressed controls (TD-con; N=28). The ASD cohort reported levels of social and non-social anhedonia that were greater than TD-con but not significantly different from TD-dep. Across cohorts, both social and non-social hedonic capacity moderated the relationship between autism symptoms and loneliness: individuals with low capacity for pleasure experienced elevated loneliness regardless of autism symptom severity, while those with intact capacity for pleasure (i.e., less anhedonia) experienced greater loneliness as a function of increased autism symptoms. Loneliness was the strongest predictor of depressive symptoms across clinical cohorts. Our findings suggest a putative pathway from trait-like anhedonia in ASD to depression via elevated loneliness and indicate that variability in hedonic capacity within the autism spectrum may differentially confer risk for depression in adults with ASD. Results underscore potential mental health benefits of social skills interventions and community inclusion programs for adults with ASD.

This cohort study uses the Vizient Clinical Data Base to compare the postoperative in-hospital morbidity and mortality of surgical patients with COVID-19 infection with patients without COVID-19 infection.

There is no clear genetic etiology or convergent pathophysiology for autism spectrum disorders (ASD). Using induced pluripotent stem cell (iPSC)-derived brain organoids and single-cell transcriptomics, we modeled alterations in the formation of the forebrain between sons with ASD and their unaffected fathers in ten families. Relative to fathers, probands with macrocephaly presented an increase in dorsal cortical plate excitatory neurons (EN-DCP) to the detriment of preplate lineages, whereas normocephalic ASD probands presented an opposite decrease in EN-DCP-related gene expression. Both cohorts converged in a dysregulation of outer radial glia genes related to translation. In macrocephalic probands, an increase in progenitor self-renewal genes ID1/ID3 was coupled to a larger pool of cortical progenitors. Furthermore, changes in ID1/ID3 expression were best predictors of ASD clinical severity. We suggest that head circumference reveals a fundamental difference in etiological mechanisms of ASD rooted in alterations in progenitor fate and unbalanced excitatory cortical neuron diversity.

BackgroundAutism spectrum disorder (ASD) is marked by repetitive thinking and high rates of depression. Understanding the extent to which repetitive negative thinking in ASD reflects autistic stereotypy versus general depressive thinking patterns (e.g., rumination) could help guide treatment research to improve emotional health in ASD. We compared associations between rumination, depressive symptoms, and pupil response to social-emotional material in adults with ASD and typically developing (TD) adults with and without depression.MethodsN = 53 verbally fluent young adults were recruited to three cohorts: ASD, n = 21; TD-depressed, n = 13; never-depressed TD-controls, n = 19. Participants completed Ruminative Response Scale and Beck Depression Inventory self-reports and a passive-viewing task employing emotionally-expressive faces, during which pupillary motility was assessed to quantify cognitive-affective load. Main and interactive effects of cohort, emotion condition, and time on pupil amplitude were tested via a linear mixed effects analysis of variance using restricted maximum likelihood estimation. Similar procedures were used to test for effects of rumination and depressive symptoms on pupil amplitude over time within ASD.ResultsResponsive pupil dilation in the ASD cohort tended to be significantly lower than TD-depressed initially but increased to comparable levels by trial end. When viewing sad faces, individuals with ASD who had higher depression scores resembled TD-depressed participants’ faster, larger, and sustained pupil response. Within ASD, depressive symptoms uniquely predicted early pupil response to sad faces, while rumination and depression scores each independently predicted sustained pupil response.ConclusionsPeople with elevated depressive symptoms appear to have faster and greater increases in pupil-indexed neural activation following sad stimuli, regardless of ASD status, suggesting the utility of conceptualizing rumination as depression-like in treatment. Ruminative processes may increase more slowly in ASD, suggesting the potential utility of interventions that decrease reactions before they are uncontrollable. Findings also reinforce the importance of testing for effects of internalizing variables in broader ASD research.

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