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Circadian Clock Dysfunction Exacerbate Autistic-Like Behaviour and Wnt/β-Catenin Signalling Dysregulation in ASD Mice

Yuxing Zhang1, Yinan Chen1,2, Wu Li1

  • 1Hunan University of Chinese Medicine, Changsha, Hunan Province, China.

Journal of Cellular and Molecular Medicine
|January 7, 2026
PubMed

Insights

Autism Spectrum Disorder (ASD) is linked to sleep issues and circadian clock disruption. Melatonin treatment improved autistic behaviors in mice by regulating the Wnt/β-catenin pathway, suggesting a therapeutic role.

Area of Science:

  • Neuroscience
  • Developmental Biology
  • Genetics

Background:

  • Sleep disturbances affect 50-80% of children with Autism Spectrum Disorder (ASD).
  • Circadian clock dysfunction and Bmal1 deficiency are implicated in ASD pathogenesis.
  • Valproic acid (VPA) exposure in mice is a model for studying ASD-like behaviors.

Purpose of the Study:

  • To investigate the role of circadian clock proteins in ASD.
  • To examine the effects of Bmal1 deficiency on VPA-induced autistic behaviors.
  • To evaluate the therapeutic potential of melatonin in an ASD mouse model.

Main Methods:

  • Characterization of circadian protein expression patterns.
  • Behavioral tests and Western blot analysis in VPA-exposed mice.
  • Bmal1 knockout and melatonin treatment in VPA-exposed mice.

Main Results:

  • VPA exposure induced autistic-like behaviors, altered circadian protein expression, and disrupted Wnt signaling.
  • Bmal1 knockout exacerbated behavioral deficits and Wnt pathway impairment in VPA-exposed mice.
  • Melatonin treatment reversed Wnt downregulation and improved behaviors in VPA-exposed mice.

Conclusions:

  • Circadian dysregulation plays a role in ASD pathogenesis.
  • Melatonin shows therapeutic potential for ASD-like behaviors via Wnt/β-catenin pathway modulation.
  • Bmal1 may function as a co-activator in the Wnt-β-catenin signaling pathway.

Keywords:
Bmal1Wnt/β‐catenin signallingautism spectrum disorderscircadian rhythmmelatonin

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