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REV-ERB-alpha and -beta coordinately regulate astrocyte reactivity and proteostatic function.

Collin J Nadarajah1, Michelle Y Li1, Elsa I Quillin1

  • 1Department of Neurology, Washington University School of Medicine, St. Louis, MO 63110.

Proceedings of the National Academy of Sciences of the United States of America
|January 30, 2026
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Summary
This summary is machine-generated.

The study reveals that REV-ERB nuclear receptors regulate astrocyte function and brain health. Dual deletion of REV-ERB-α and REV-ERB-β in astrocytes mitigates Parkinson

Keywords:
REV-ERBalphaalpha-synucleinastrocytecircadianneuroinflammation

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Chronobiology

Background:

  • The molecular circadian clock regulates central nervous system (CNS) functions, including glial responses and neurodegenerative pathology.
  • Nuclear receptors REV-ERB-α (Nr1d1) and REV-ERB-β (Nr1d2) are core circadian clock components influencing metabolism, neuroinflammation, synaptic pruning, and protein aggregation.
  • The cell-type-specific roles and compensatory effects of REV-ERB-α and REV-ERB-β in the brain remain largely unknown.

Purpose of the Study:

  • To investigate the CNS functions of REV-ERB nuclear receptors.
  • To elucidate the cell type-specific roles and compensatory effects of REV-ERB-α and REV-ERB-β in the brain.
  • To explore the therapeutic potential of REV-ERBs in neurodegenerative diseases.

Main Methods:

  • Development of mouse models with global or astrocyte-specific conditional knockout of REV-ERB-α and REV-ERB-β.
  • Analysis of transcriptional changes in the brain following inducible postnatal global deletion of REV-ERBs.
  • Investigation of astrocyte reactivity and STAT3 signaling pathways.
  • In vitro and in vivo assessment of alpha-synuclein uptake, degradation, and pathology spreading.

Main Results:

  • Inducible global deletion of REV-ERB-α and REV-ERB-β induced extensive transcriptional changes in disease-relevant pathways and spontaneous astrocyte reactivity.
  • Astrocyte-specific deletion of REV-ERBs recapitulated astrocyte reactivity, indicating cell-autonomous regulation.
  • REV-ERB-α/-β were found to repress STAT3 transcription, and their deletion induced STAT3 expression in astrocytes.
  • Dual REV-ERB deletion enhanced astrocyte alpha-synuclein uptake and degradation, and mitigated alpha-synuclein spreading in a Parkinson's disease model.

Conclusions:

  • REV-ERBs are critical regulators of astrocyte function and activation.
  • Astrocyte REV-ERBs act downstream of the core circadian clock to control astrocyte reactivity via STAT3 signaling.
  • Targeting astrocyte REV-ERBs offers a potential therapeutic strategy for synucleinopathies and other neurodegenerative pathologies.