Recent studies suggest that glutamate (GLU) signaling abnormalities are involved in the etiology of Autism Spectrum Disorder (ASD), suggesting perturbations in GLU and glutamine (GLN) metabolism. Although GLU and GLN plasma concentrations have been linked to cognitive decline, the actual production of GLU and GLN have never been measured in ASD and linked to ASD severity score and neurocognitive and mood changes.
19 young adults with high functioning ASD (age 24.3 ± 1.0y, Autism Quotient (AQ): 31.4 ± 1.7), and 46 control subjects (age 23.4 ± 0.3y)) were enrolled. ASD severity and subscores as well as cognitive function and mood were assessed (MOCA, TMT, word fluency, Stroop, HADS). Postabsorptive amino acid kinetics (production of GLU and GLN, and its interconversion rates (GLU <
No differences were present in word fluency, but higher values in ASD for TMTb (p = 0.066), depression (p = 0.0004), anxiety (p = 0.0006) and lower values for MOCA (0.0054). The ASD group was characterized by lower plasma GLN and GLU concentrations (p > 0.05). Although the production rates of GLN and GLU were not different between the groups, in ASD GLN <
Disturbances in GLN and GLU metabolism in ASD are associated with changes in ASD subscores but less with neurocognitive dysfunction or mood changes.