Abstract
Autism spectrum disorder (ASD) is a neurodevelopmental disorder characterized by defective social communication and interaction and restricted, repetitive behavior with a complex, multifactorial etiology. Despite an increasing worldwide prevalence of ASD, there is currently no pharmacological cure to treat core symptoms of ASD. Clinical evidence and molecular data support the role of impaired mitochondrial fatty acid oxidation (FAO) in ASD. The recognition of defects in energy metabolism in ASD may be important for better understanding ASD and developing therapeutic intervention. The nuclear peroxisome proliferator-activated receptors (PPAR) α, δ, and γ are ligand-activated receptors with distinct physiological functions in regulating lipid and glucose metabolism, as well as inflammatory response. PPAR activation allows a coordinated up-regulation of numerous FAO enzymes, resulting in significant PPAR-driven increases in mitochondrial FAO flux. Resveratrol (RSV) is a polyphenolic compound which exhibits metabolic, antioxidant, and anti-inflammatory properties, pointing to possible applications in ASD therapeutics. In this study, we review the evidence for the existing links between ASD and impaired mitochondrial FAO and review the potential implications for regulation of mitochondrial FAO in ASD by PPAR activators, including RSV.
Highlights
Autism spectrum disorder (ASD) is a lifelong condition characterized by persistent deficits in social communication and social interaction across multiple contexts and restricted and/or repetitive patterns of behavior and/or activities that must be present in the early developmental period [1]
By a naïve Bayes algorithm, we found an increased performance of the algorithm based on the identified acyl-carnitines for classifying ASD in toddlers (n: 42 subjects; mean age 3.26 ± 0.89) with 72.3% sensitivity, 72.1% specificity, and diagnostic odds ratio (DOR) of 11.25
Prenatal exposure to RSV attenuates the ASD-like behavior in the model induced by prenatal exposure to valproic acid (VPA), the molecular mechanisms mediating the effects at the cellular level are still largely undiscovered [42]
Summary
Autism spectrum disorder (ASD) is a lifelong condition characterized by persistent deficits in social communication and social interaction across multiple contexts and restricted and/or repetitive patterns of behavior and/or activities that must be present in the early developmental period [1]. 2. Autism Spectrum Disorder in Genetic Diseases of Mitochondrial Fatty Acid β-Oxidation mtFAO represents a major source of ATP in various tissues with high energy demand, in particular the heart, skeletal muscle, and liver, when fasting or prolonged exercise requires glucose sparing. Autism Spectrum Disorder in Genetic Diseases of Mitochondrial Fatty Acid β-Oxidation mtFAO represents a major source of ATP in various tissues with high energy demand, in particular the heart, skeletal muscle, and liver, when fasting or prolonged exercise requires glucose sparing In these situations, adipose tissue lipolysis makes free fatty acids available for mitochondrial β-oxidation, providing acetyl-CoA that enters the tricarboxylic acid (TCA) cycle for complete oxidation. The acyl-carnitines profile observed in subsets of ASD patients and in PPA rodent ASD model support the hypothesis of a partial mtFAO deficiency, but it appears relatively atypical compared to the profiles observed in inborn monogenic disorders affecting one of the enzymes in the mtFAO pathway. Partial defects in mtFAO can be related to respiratory chain (RC) dysfunction, since there are strong functional links between the mtFAO and RC pathways and increasing evidence shows that mitochondrial dysfunction associated with ASD includes deficient activity levels of both the mitochondrial RC and FAO pathways [77,78]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
