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Effects of overweight or obesity on resting state functional connectivity of brains of children with autism spectrum disorder

Fri, October 5, 1:15 to 2:45pm, Doubletree Hilton, Room: Tempe

Abstract

Background: Autism spectrum disorder (ASD) is a developmental disorder characterized by difficulties in communication, social interaction, and restricted repetitive behaviors. ASD is often associated with an increased risk of development of overweight or obesity (OWOB). Resting state functional connectivity of the brains of children with ASD, OWOB and their coexistence have not been studied.
Methods: Publically available, de-identified, phenotypic data and preprocessed resting state functional magnetic resonance imaging (rs-fMRI) data shared via the Autism Brain Imaging Data Exchange (ABIDE) Preprocessed initiative were accessed. Records of children (i.e. age < 18 years) with biologically plausible body mass indices (BMI) were identified and their rs-fMRI data preprocessed using the Connectome Computation System pipeline and mean time series for the bilateral orbitofrontal cortex (OFC), middle frontal gyrus (MFG), and medial frontal cortex (MFC) seed regions were downloaded. Presence of OWOB (i.e. BMI ≥ 85th centile for age and sex) was determined using CDC BMI for age charts. Subject level correlations between each seed region’s time series and rs-fMRI data of the entire brain were analyzed using the Feat tool in FSL. Group-level analyses were performed to compare the groups with 1) ASD but not OWOB, 2) OWOB but not ASD and 3) both conditions with the group without ASD or OWOB (i.e. controls) using a factorial regression model controlling for sex, age and study site. Final statistical maps were thresholded using a permutation-based approach in FSL (i.e. randomise).
Results: BMI was available for 81 children (11.97 ±2.77 years; 59 male; 37 with ASD; 24 with OWOB). Evidence of hypo-connectivity between R/OFC and a cluster that included the posterior node of the default mode network; DMN (i.e. precuneus) was observed in the group with ASD without OWOB compared to the controls (P = 0.003; FWER). In contrast, the group with both ASD and OWOB showed hyper-connectivity between the R/OFC and a cluster that included the posterior node of the DMN (P = 0.015; FWER).
Conclusion: Previous evidence suggests that strength of rs-fMRI connectivity between OFC and posterior DMN is negatively associated with ASD symptom severity. Our observation of hypo-connectivity between the OFC and the posterior DMN in isolated ASD is consistent with these findings. Observed hyper-connectivity between these regions in coexistence of ASD and OWOB suggests that weight gain may be associated with better symptomatic outcomes in ASD. More evidence is needed to confirm this hypothesis and further explicate any causal inferences.

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