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Establishing a Device for Sleep Deprivation in Mice
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Published on: September 22, 2023

Peripheral metabolic dysfunction drives sleep disruption in TDP-43 proteinopathy.

Anyara Rodriguez1, Samuel J Belfer1, Jenny Luong1

  • 1Department of Psychiatry, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, PA, 19104, USA.

Biorxiv : the Preprint Server for Biology
|May 13, 2026
PubMed
Summary

Neurodegenerative diseases like TDP-43 proteinopathy cause sleep loss due to peripheral metabolic dysfunction, not just brain issues. Restoring metabolic health, particularly through SIK3, can rescue sleep patterns.

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Area of Science:

  • Neuroscience
  • Metabolic research
  • Genetics

Background:

  • Sleep disruption is an early symptom of neurodegenerative diseases.
  • Current understanding attributes sleep loss to neuronal dysfunction or cell death.
  • The link between metabolic state and sleep suggests systemic metabolic abnormalities could be involved.

Purpose of the Study:

  • To investigate if peripheral metabolic dysfunction causally contributes to sleep disruption in TDP-43 proteinopathy models.
  • To identify molecular mechanisms linking metabolic state and sleep loss.

Main Methods:

  • Utilized *Drosophila* models of TDP-43 proteinopathy.
  • Induced metabolic changes through genetic manipulation and dietary interventions.
  • Conducted RNAi screening to identify genetic modifiers.
  • Performed transcriptomic and spatial metabolomic analyses.

Main Results:

  • TDP-43 expression induced a starvation-like metabolic state with depleted energy stores despite normal feeding.
  • Sleep restoration drugs did not fix metabolic defects, but metabolic interventions rescued sleep.
  • SIK3 was identified as a key suppressor of sleep loss and starvation sensitivity.
  • SIK3 remodeled peripheral metabolism via the pentose phosphate pathway and redox metabolites.

Conclusions:

  • Systemic metabolic dysfunction is a primary driver of sleep disruption in TDP-43 proteinopathy.
  • Peripheral metabolism represents a potential therapeutic target for sleep disturbances in neurodegenerative diseases.