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Cognitive Control Development in Autism Spectrum Disorder: Can Rdoc Help Us to Better Understand Behavioral Phenotypes and Pathophysiology?
Many individuals with Autism Spectrum Disorder (ASD) exhibit executive function deficits which persist into adolescence and young adulthood, and map closely to RDoC Matrix components of cognitive control (CC). Adolescents and young adults with typical development (TYP), show significant increases in functional connectivity (fc) between the lateral prefrontal (LPFC) and parietal cortices which is thought to permit mature levels of goal maintenance and response inhibition. Implementing an RDoC perspective to examine CC development holds the potential to provide insights related to ASD phenotypes, pathophysiology, and treatment-matching.
Objectives:
To initiate an RDoC-oriented examination of CC in ASD by: 1) Determining the proportion of those with ASD who are impaired in CC compared to those with TYP, 2) Investigating the neural correlates of cognitive control in ASD who are compared to those with TYP with better and poorer task performance, and 3) Examining whether the reduced fronto-parietal connectivity associated with attention deficit hyperactivity disorder (ADHD) symptoms is also found in ASD (Solomon et al., 2009).
Methods:
Participants included 56 individuals with ASD (mean age = 18.4; mean IQ = 104), and 70 individuals with TYP (mean age = 18; mean IQ = 109) from the first wave of a cohort-sequential study of CC in youth ages 12-22 years. We implemented a rapid event-related version of the Preparing to Overcome Prepotency (rPOP) task during scanning. Seed to voxel whole brain fc analyses were implemented using PPI in the CONN fc toolbox (http://www.nitrc.org /projects/conn). Dorsolateral prefrontal cortex (DLPFC) and dorsal anterior cingulate (dACC) seeds were used. ADHD symptoms were assessed using the ASEBA.
Results:
Both ASD and TYP were slower to respond to red versus green trials, with a greater RT difference in ASD (F(1, 123) = 4.4, p<.05). Two thirds of participants with ASD showed red-green RT greater than the TYP mean and were grouped as poorer performers (n=37; ASD-poorer); remaining participants were grouped as better performers (n=19; ASD-better). There were no univariate differences in neural activation between ASD or TYP. TYP versus ASD-better showed greater recruitment of temporal cortical regions at the cue, with no other diagnostic group differences across the performance groups. TYP exhibited more extensive fc between CC network regions than ASD throughout the task, while ASD showed more connectivity between prefrontal and posterior regions that was inversely associated with task performance. At the probe, TYP versus ASD also showed increased DLPFC fc with the insula and left inferior frontal gyrus. ASD-better showed fc more similar to TYP. Fronto-parietal connectivity was not associated with ADHD symptoms.
Conclusions:
CC deficits were not universal in ASD. Univariate analyses illustrated that the ASD, TYP, and better and poorer performers, exhibited minimal differences in neural recruitment during the task. Greater differences were found in fc where TYP engaged more extensive networks traditionally associated with preparatory control (ACC, parietal cortex), and response inhibition (insula), which were also used by ASD-better. Results thus far, suggest that support for RDoC CC in ASD is equivocal, however, developmental and other analyses are ongoing.