557. GLUTAMATE, GLUTAMINE, AND GABA LEVELS IN ADULTS WITH AUTISM SPECTRUM DISORDER: A 7T MRS STUDY

Abstract Background Alterations in excitatory and inhibitory neuronal tones are implicated in the pathophysiology of autism spectrum disorder (ASD). Excitatory neurotransmission is primarily mediated by glutamate (Glu) and its precursor, glutamine (Gln), whereas inhibitory neurotransmission is mediated by GABA. Magnetic resonance spectroscopy (MRS) at 7T MR enables the in vivo assessments of neurometabolites, including Glu, Gln, and GABA, with increased sensitivity. Aims & Objectives We aimed to investigate the status of Glu, Gln, and GABA in the brain of adults with ASD, using MRS with a 7T MR device. Method Thirty-three adults with ASD (mean age = 31.1 years) and 52 neurotypical control adults were included in this study. MRS scans of all participants were conducted using the semi-adiabatic short TE spin-echo full-intensity-acquired localized single voxel spectroscopy (sSPECIAL) sequence. The volumes of interest (VOIs) were localized at the anterior cingulate cortex (ACC), the bilateral thalamus, and the right temporo-parietal junction (TPJ). MRS quantification was conducted with LCModel, and quality control of the data was performed. Analysis of covariance (ANCOVA) was conducted to examine the effects of diagnosis on Glu, Gln, and GABA levels in each VOI, controlling for age and sex. Statistical significance thresholds were set at p < 0.05, with Bonferroni correction for the three VOIs. Results ANCOVA demonstrated significant effects of diagnosis on Gln for the thalamus (p = 0.012) and the right TPJ (p = 0.006), and a trend for the ACC (p = 0.04), indicating that Gln levels in these regions are higher in the ASD group. No significant effects of diagnosis were found on either Glu or GABA. Discussion & Conclusions The current results indicate that alterations in the regulation of excitatory neurotransmission, presumably increased cycling of the Gln-Glu circuit, may underlie the pathophysiology of ASD.