Abstract

Summary

This thesis investigated whether shared SCN histopathology underlies circadian dysfunction in mouse models of Rett syndrome, Autism Spectrum Disorder, and Huntington's disease, finding no common anatomical phenotype. This suggests that lighting and circadian interventions for these conditions may need to target disease-specific mechanisms rather than a shared SCN pathway.
Abstract

Key Findings

  • No common histoanatomical phenotype was observed in the SCN across mouse models of Rett syndrome, ASD, and Huntington's disease.
  • Nissl staining revealed no gross morphological changes in SCN structure across the three models.
  • Immunohistochemistry found no consistent loss of SCN neuropeptide-expressing neuron subpopulations, suggesting distinct underlying circadian disruption mechanisms per disease.
Categories

Categories

The Science of Light: Examines the suprachiasmatic nucleus (SCN), the central circadian clock, for histopathological changes that could explain circadian dysfunction across neurological diseases.
Dementia & Elder Care: Investigates circadian disturbances in Huntington's disease, a neurodegenerative condition, at the level of SCN neuropeptide-expressing neuron populations.
Authors

Author(s)

ZA MacDowell Kaswan
Publication Date

Publication Year

2016
View more publications