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Altered oscillatory coupling reflects possible inhibitory interneuron dysfunction in Rett syndrome.

Devorah Kranz1,2,3, Yael Braverman1, Michelle McCarthy3,4

  • 1Boston Children's Hospital, Boston, MA 02115.

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|August 8, 2025
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Summary
This summary is machine-generated.

Rett syndrome shows altered brain activity, specifically increased phase-amplitude coupling, linked to VIP interneuron dysfunction. This finding may offer a biomarker for cortical dysfunction and guide new therapeutic targets.

Keywords:
EEGRett syndromeVIP+ interneuronsneurogenetic disordersphase-amplitude coupling

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Area of Science:

  • Neuroscience
  • Computational Neuroscience
  • Genetics

Background:

  • Rett syndrome, a neurodevelopmental disorder caused by MECP2 gene variants, results in cognitive impairments.
  • Understanding large-scale brain dynamics via neural oscillations is crucial for studying Rett syndrome.
  • Phase-amplitude coupling (PAC) is a key cross-frequency interaction for information integration, potentially revealing neural dysfunction.

Purpose of the Study:

  • To investigate alterations in phase-amplitude coupling (PAC) in Rett syndrome.
  • To explore the underlying cellular and circuit-level mechanisms of PAC changes.
  • To identify potential biomarkers and therapeutic targets for Rett syndrome.

Main Methods:

  • Recorded resting-state EEG from individuals with Rett syndrome and controls.
  • Quantified PAC strength (modulation index) and phase bias.
  • Modeled a biophysically-constrained cortical network to identify mechanisms.

Main Results:

  • Significantly stronger PAC in Rett syndrome across widespread cortical regions and frequency pairs (e.g., theta-gamma, alpha-gamma).
  • Increased theta-gamma and alpha-gamma coupling observed in anterior, posterior, and whole-brain regions.
  • Biophysically constrained modeling indicated reduced VIP-expressing interneuron activity could explain observed PAC alterations.

Conclusions:

  • Identified altered awake-state PAC in Rett syndrome, mechanistically linked to VIP+ interneuron dysfunction.
  • Elevated PAC may serve as a biomarker for cortical dysfunction and bridge neural circuitry to EEG signatures.
  • Results suggest VIP+ interneurons as a target for novel therapeutic interventions in Rett syndrome.