Atypical development of resting-state periodic and aperiodic EEG activity in 22q11.2 deletion syndrome

22q11.2 deletion syndrome (22q11DS) carries increased psychosis risk, making it a valuable model for identifying neurobiological markers. Electrophysiological alterations similar to idiopathic psychosis have been reported, particularly in gamma-band oscillations. However, the aperiodic 1/f component, a putative marker of excitatory-inhibitory balance, is rarely separated from periodic activity, and the developmental trajectories of both remain largely unexplored in 22q11DS.

This longitudinal study included 117 individuals with 22q11DS and 96 healthy controls (HC), aged 6-35 years, totaling 451 eyes-closed resting-state EEG recordings. Spectral relative power (RP) was computed across six frequency bands over whole scalp, frontal, and occipital electrodes. Aperiodic exponent and offset were extracted across the whole scalp. Mixed-model regression analyses examined developmental trajectories in 22q11DS and HC.

Deletion carriers showed atypical trajectories across frequency bands. From adolescence, frontal delta RP declined more steeply, whereas beta and low-gamma RP showed more pronounced and widespread increases compared to HC. Moreover, a consistently higher aperiodic offset was found in 22q11DS. While periodic and aperiodic components did not distinguish participants with and without psychotic symptoms, lower low-gamma power was associated with higher symptom severity.

Atypical maturation of neural oscillations emerged from adolescence in 22q11DS, particularly in delta, beta, and low-gamma frequencies. A higher aperiodic offset may reflect elevated broadband neural activity, while the preserved exponent suggests that group differences are primarily driven by periodic changes. Elevated low-gamma may represent a neurodevelopmental marker of psychosis vulnerability, whereas its inverse association with symptom severity points to stage-dependent gamma alterations consistent with idiopathic psychosis.