<p>Using a set of inflammatory markers, we identified a cluster of patients with autism spectrum disorders (ASD) and high levels of inflammation (<i>n</i> = 35, 70%). Discriminant analysis showed that quinolic acid, the catabolite of the kynurenine pathway, makes the greatest contribution to the pathogenesis of ASD. Dysregulation of energy metabolism has been revealed, including both the main pathways of catabolism (glycolysis, the Krebs cycle) and alternative pathways (beta-oxidation, ketogenesis, branched amino acid metabolism) with impaired mitochondrial function (meglutol) in patients with ASD. Correlations have been revealed for a number of energy exchange metabolites with indices of inflammation. Inflammation in ASD is associated with dysregulation of energy metabolism and mitochondrial dysfunction. These data can serve as the basis for new treatment protocols, including anti-inflammatory therapy, metabolic correction, and restoration of mitochondrial function.</p>

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The Relationship of Inflammation with Energetic Metabolism and Mitochondrial Dysfunction in Autistic Spectrum Disorders

  • V. O. Generalov,
  • T. P. Klushnik,
  • T. E. Obodzinskaya,
  • G. V. Larionov,
  • A. N. Aleksandrenkova,
  • T. R. Sadykov,
  • A. M. Yugai,
  • Yu. V. Kazakova,
  • L. A. Mamedov

摘要

Using a set of inflammatory markers, we identified a cluster of patients with autism spectrum disorders (ASD) and high levels of inflammation (n = 35, 70%). Discriminant analysis showed that quinolic acid, the catabolite of the kynurenine pathway, makes the greatest contribution to the pathogenesis of ASD. Dysregulation of energy metabolism has been revealed, including both the main pathways of catabolism (glycolysis, the Krebs cycle) and alternative pathways (beta-oxidation, ketogenesis, branched amino acid metabolism) with impaired mitochondrial function (meglutol) in patients with ASD. Correlations have been revealed for a number of energy exchange metabolites with indices of inflammation. Inflammation in ASD is associated with dysregulation of energy metabolism and mitochondrial dysfunction. These data can serve as the basis for new treatment protocols, including anti-inflammatory therapy, metabolic correction, and restoration of mitochondrial function.