Reduced REM sleep fast theta power suggests early circuit vulnerability in a GBA1 mouse model of prodromal synucleinopathy

Sleep disturbance is a salient harbinger of synucleinopathies and is conspicuous in idiopathic REM sleep behaviour disorder. Variants in GBA1 confer substantial risk for iRBD and Parkinson’s disease, yet early electrophysiological correlates remain uncertain. We recorded 24‑h EEG/EMG in adult male D409V/WT GBA1 knock‑in and wild‑type mice. A priori, REM fast‑theta (8–10 Hz) relative power was the primary endpoint, tested in an epoch‑level linear mixed‑effects model with a random intercept per animal and fixed effects of genotype, light phase, and their interaction. Secondary bands were slow‑theta (5–7 Hz), total theta (5–10 Hz) and delta (1–4 Hz). Aperiodic components (offset, exponent) were parameterised with FOOOF (fixed mode, 2.5–40 Hz). Fast‑theta during REM was lower in GBA1 heterozygotes (β≈−0.013; p ≈ 0.032), though the genotype effect did not survive Benjamini–Hochberg false‑discovery control across the REM‑band family (q ≈ 0.127). Sensitivity analyses aligned in direction: clustered‑SE OLS and a non‑parametric Bayesian bootstrap on per‑animal values both supported a fast‑theta reduction, while slow‑theta, total theta and delta showed no group differences. Sleep macroarchitecture and aperiodic activity were similar between genotypes. This indicates a frequency‑specific attenuation of REM fast‑theta early in GBA1 heterozygotes, with preserved aperiodic background and architecture. Selective fast-theta attenuation may signal early microphysiological circuit vulnerability.