Exploring Shared Mechanisms across Autism and Depression to Inform Emotional Health Interventions in ASD

Background: Depression is a leading form of clinical impairment for adults with ASD, with reported rates as high as 38-70% in convenience samples. Depressed mood in ASD impairs daily functioning, heightens the need for special services and medications, and places an increased burden on caregivers. By learning about the phenomenology and causal pathways of depression in ASD, we can begin to develop screening, assessment, and intervention protocols tailored to the specific needs of this population, particularly underserved adults with ASD.

Objectives: To identify potential contributors to depressed mood in ASD by comparing adults with ASD, typically developing adults with depressive disorders (TD-dep), and never-depressed controls (TD-con) on several phenomena associated with depression, including repetitive thinking, attentional bias and neural response to negative emotional material, and social anhedonia.

Methods: Our current sample of n=112 will increase significantly by May 2018. This abstract reflects findings from manuscripts in preparation based on a preliminary subset of n=53 adults aged 18-35 with verbal IQ>80. Cohorts included ASD (n=21), TD-dep (n=13), and TD-con (n=19). Participants completed diagnostic assessments (including the Autism Diagnostic Observation Scale, second edition, and the Structured Clinical Interview for DSM-5 Disorders), self-report questionnaires (e.g., Beck Depression Inventory; Ruminative Response Scale; Anticipatory and Consummatory Interpersonal Pleasure Scale), and passive-viewing tasks employing emotionally-expressive faces, during which (1) pupil motility was used to index cognitive-emotional load in response to single faces emoting happy, sad, neutral, or angry expressions presented for 400 milliseconds then masked for 9 seconds, and (2) visual attention to emotional over neutral faces was quantified in a paired preference eye-tracking task.

Results: (1) When looking at brief-then-masked emotional faces, people with elevated depressive symptoms had faster, greater, and longer-lasting increases in pupil-indexed neural activation to sad stimuli regardless of ASD status (Figure 1.A). (2) Within ASD, distinct profiles of pupil response differentiated rumination in the context of depression versus general repetitive thinking (Figure 1.B). (3) The ASD group displayed significantly faster fixations to sad over neutral faces (t =-3.66, p=.002), and those with greater repetitive thinking spent more overall time on sad than neutral faces (Cohen’s d=.90, large effect); (4) Both the ASD and TD-dep groups displayed significantly decreased preference for happy faces compared to TD-con (F=15.79, p<.001; Figure 2). (5) Participants with ASD exhibited a similar pattern of social reward functioning as TD-dep, in which greater social ‘wanting’ was associated with the experience of loneliness and depressive symptoms.

Conclusions: We observed several parallels in cognitive, attentional, and emotional processing across our ASD and TD-dep samples in comparison to TD-controls. Specific findings indicate that rumination, negative attention bias, and social anhedonia may be best conceptualized as “depression-like” (rather than autism-specific) in treatment for adults with ASD. We also noted that our pupil results begin to isolate potential biomarkers of depression-specific and autism-specific cognitive-emotional processing. We will discuss existing treatments for rumination that may be adapted for the ASD population, as well as reward-based social skills training that may enhance emotional well-being in adults with ASD.