ABSTRACT
OBJECTIVE: To study the relationship of N-acetylaspartate (NAA) metabolism and choline (Cl) metabolism in different parts of the brain based on magnetic resonance spectrography (1H-MRS) with clinical manifestations of autism spectrum disorders (ASD). MATERIAL AND METHODS: Twenty-two children (16 boys, 6 girls), aged 2-10 years, were studied. Russian-language adapted versions of the Autism Treatment Evaluation Checklist (ATEC) and the Nisonger Child Behavior Rating Form (NCBRF) were administered. The ratio of metabolites NAA/creatine (Cr), Cho/Cr, Cho/NAA in the prefrontal cortex, postcentral gyrus and temporal lobes was studied using 1H-MRS. RESULTS: The following correlations were found: 1) between the NAA/Cr value and the Sensory/Cognitive Awareness scale in the prefrontal cortex on the left (ρ=0.479) and on the right (ρ=0.483); the Health/Physical Behavior scale in the precentral gyrus on the left (ρ=0.572) and on the right (ρ=0.463); the Sociability scale in the temporal lobe on the left (ρ=0.481) and on the right (ρ=0.796); the Speech/Language/Communication scale in the right temporal lobe (ρ=-0.552); 2) between the Cho/Cr value and the Adaptive Social scale in the postcentral gyrus on the left (ρ=-0.466) and on the right (ρ=-0.518); the Compliant/Calm scale in the prefrontal cortex on the right (ρ=0.624) and on the left (ρ=-0.541); 3) between the Cho/NAA ratio and the Speech/Language/Communication scale in the right pre-central (ρ=-0.471) and post-central gyrus (ρ=-0.507); the Self-Isolated/Ritualistic¼ scale in the left (ρ=-0.486) and right temporal lobe (ρ=-0.596). CONCLUSIONS: Thus, the predominant localization of disorders of N-acetylaspartate metabolism in communication disorders (bilaterally in the temporal lobes), cognitive, behavioral and somatic manifestations (bilaterally in the prefrontal regions) was established. Increased CI metabolism has identified deficits in interaction skills in both postcentral gyrus, and reveals bilateral differences in the effect on behavioral control in the prefrontal cortex. The results confirm the previously established numerous patterns between abnormal activation of the prefrontal cortex and neuronal dysfunction in ASD. But unlike other studies, it was possible to trace these relationships within a narrower phenotype of disorders - atypical autism comorbid with psychomotor disinhibition.
Subject(s)
Autistic Disorder , Aspartic Acid , Brain , Choline , Creatine , Female , Humans , Magnetic Resonance Spectroscopy , Male , Proton Magnetic Resonance SpectroscopyABSTRACT
Objective:To explore the mechanism of Sailuotong capsules in treating acute cerebral ischemia from the perspective of metabonomics. Method:A total of 24 SD rats were randomly divided into 3 groups, including sham-operated group, model group and Sailuotong group (33 mg·kg-1). The rat model of acute multiple cerebral infarction was established by injecting fluorescent microspheres into internal carotid artery. After the successful operation, rats in Sailuotong group were administered by duodenal injection immediately, and the dosage volume was 2 mL·kg-1. Endogenous metabolites in rat brain tissues of each group were determined by UPLC-Q-TOF-MS. The relevant data and biomarkers were analyzed by principal component analysis (PCA) and partial least squares-discriminant analysis (PLS-DA). Result:The analysis of pattern recognition indicated that the metabolite profiles in model group and sham-operated group were separated obviously, and ten biomarkers related to acute cerebral ischemia were also identified. Compared with the sham-operated group, contents of N-acetylaspartate (NAA), fumaric acid, glutathione, dehydroascorbic acid, aspartic acid and S-adenosylhomocysteine were decreased, while the contents of arginine, citrulline, saccharopine and hydantoin-5-propionic acid were increased in the model group. Meanwhile, the ten abnormal biomarkers mentioned above got restoration in Sailuotong group. Conclusion:The main regulated metabolic pathways of Sailuotong capsules are NAA metabolism, arginine metabolism, energy metabolism, oxidative stress, etc.
