The influence of circadian rhythms and aerobic glycolysis in autism spectrum disorder.

Transl Psychiatry

DACTIM-MIS, Laboratory of Mathematics and Applications (LMA), UMR CNRS 7348, University of Poitiers, Poitiers, France.

Published: November 2020

AI Article Synopsis

  • Intellectual abilities and clinical presentations in autism spectrum disorder (ASD) vary widely, and the causes of ASD are still not fully understood.
  • ASD is often linked to sleep disorders and involves complex biological rhythms that influence brain development and behavior.
  • Recent research highlights that the dysregulation of circadian rhythms affects the WNT/β-catenin signaling pathway, which may contribute to metabolic changes and cognitive issues in individuals with ASD.

Article Abstract

Intellectual abilities and their clinical presentations are extremely heterogeneous in autism spectrum disorder (ASD). The main causes of ASD remain unclear. ASD is frequently associated with sleep disorders. Biologic rhythms are complex systems interacting with the environment and controlling several physiological pathways, including brain development and behavioral processes. Recent findings have shown that the deregulation of the core clock neurodevelopmental signaling is correlated with ASD clinical presentation. One of the main pathways involved in developmental cognitive disorders is the canonical WNT/β-catenin pathway. Circadian clocks have a main role in some tissues by driving circadian expression of genes involved in physiologic and metabolic functions. In ASD, the increase of the canonical WNT/β-catenin pathway is enhancing by the dysregulation of circadian rhythms. ASD progression is associated with a major metabolic reprogramming, initiated by aberrant WNT/β-catenin pathway, the aerobic glycolysis. This review focuses on the interest of circadian rhythms dysregulation in metabolic reprogramming in ASD through the aberrant upregulation of the canonical WNT/β-catenin pathway.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7669888PMC
http://dx.doi.org/10.1038/s41398-020-01086-9DOI Listing

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