Effects of Overweight or Obesity on Brain Structural Connectivity of Children with Autism Spectrum Disorders

• In Event: Poster Session 12
  In Poster Session: PS 12 Topic - Biological Processes: Neuroscience and Genetics

Abstract

Background: Children with autism spectrum disorders (ASD) are at a higher risk of developing overweight or obesity (OWOB). ASD and OWOB each are associated with abnormalities in resting state functional magnetic resonance imaging (rs-fMRI) connectivity of the brain. Specifically, rs-fMRI connectivity of anterior and posterior nodes of the default mode network (DMN) is negatively associated with ASD severity and presence of OWOB in ASD seem to reverse this functional dissociation. However, the independent and combined effects of ASD and OWOB on intrinsic structural (i.e., white matter) connectivity of DMN have not been examined. Therefore, in a secondary analysis of diffusion tensor imaging (DTI) data, we explored the effects of ASD, OWOB and their interaction on structural connectivity between anterior and posterior nodes of DMN.
Methods: De-identified phenotypic and DTI data of children (i.e., age < 18 years) with and without ASD with a record of body mass index (BMI) were downloaded from the Autism Brain Imaging Data Exchange (ABIDE) II database. Children with BMI > 85th percentile for age and sex based on CDC charts were coded as having OWOB. DTI data were subjected to distortion correction and brain extraction and were subsequently corrected for eddy currents and head motion using tools in the FDT Toolbox in FSL. The diffusion parameters of the images were estimated using a Bayesian approach (i.e., BEDPOSTX) in FSL. Waypoint connectivity mapping was performed to estimate the connectivity between the anterior and posterior nodes of DMN of each subject using probabilistic tractography. (i.e., PROBTRACX) in FSL. The effects of ASD, OWOB and their interaction on total anterior-posterior DMN structural connectivity strength was examined in a two-way ANOVA and subsequent post-hoc comparisons were adjusted for FWER using Tukey’s correction.
Results: Records of 67 children (age 8.05±1.93 years; 61 males; 46 with ASD; 16 with OWOB) met eligibility. Two-way ANOVA of anterior-posterior total DMN connectivity revealed significant main effects for ASD (F1,63 = 4.544, p = 0.037) and OWOB (F1,63 = 4.440, p = 0.039) and a significant ASD x OWOB interaction (F1,63 = 6.969, p = 0.010). Specifically, anterior-posterior DMN connectivity was decreased in children with ASD compared to neurotypical children (Δ = -119490.7 [-231815.5, -7165.867]) and the was increased in children with OWOB compared to children with a normal weight (Δ = 128868.6 [6655.1, 251082.1]). Exploration of the significant interaction revealed no differences between anterior-posterior DMN connectivity among subgroups of children with ASD and OWOB, with ASD without OWOB or without ASD or OWOB. However, all of the above groups showed significantly lower anterior-posterior DMN structural connectivity compared to neurotypical children with OWOB (p = 0.007, p = 0.001, and p = 0.009, respectively).
Conclusions: Observed decreased intrinsic structural connectivity of DMN in children with ASD corresponds to the previously observed impaired intrinsic rs-fMRI connectivity of DMN. While presence of OWOB among children with ASD was observed to reverse the aberrant intrinsic rs-fMRI connectivity of DMN, this OWOB associated functional improvement is unlikely to be due to an underlying increase in structural connectivity.

Authors

• Chanaka Kahathuduwa, Texas Tech University Health Sciences Center
  Non-Presenting Author

• Chathurika S Dhanasekara, Texas Tech University Health Sciences Center
  Non-Presenting Author

• Sarah M Wakefield, Texas Tech University Health Sciences Center
  Non-Presenting Author

• Ann M Mastergeorge, Texas Tech University
  Presenting Author