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Figure 8 | Molecular Autism

Figure 8

From: Antipurinergic therapy corrects the autism-like features in the Fragile X (Fmr1 knockout) mouse model

Figure 8

Metabolic pathways shared by the MIA and Fragile X mouse models and human ASD. Comprehensive metabolomic analysis identified 20 biochemical pathways associated with symptom improvements in the Fragile X (Fmr1 knockout) model. Seventeen pathways were shared with human ASD, and 11 were shared with the maternal immune activation (MIA) model of ASD. The 17 metabolic pathways shared with human ASD were: purines, microbiome, sphingolipids, phophoslipids, cholesterol/sterols, glycolysis, Krebs cycle, vitamin B3-NAD+, pyrimidines, S-adenosyl methionine (SAM)/S-adenosylhomocysteine (SAH)/glutathione (GSH), fatty acid oxidation, eicosanoids, gangliosides, reactive oxygen species and nitric oxide (ROS/NO), branched chain amino acids, propionate metabolism and propiogenic amino acids (Ile, Val, Thr, and Met), and vitamin B6-pyridoxine metabolism. Bile acids were common to both the Fragile X and MIA models, but have not yet been studied in human autism.

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