Memory deficits link trait-like EEG spectral profiles during REM and slow-wave sleep with shared symptoms of depression and anxiety.

Emerging evidence suggests that trait-level cortical hyperarousal during sleep-indicated by heightened EEG activity in higher frequency bands-disrupts memory processing and contributes to depression and anxiety, particularly during rapid eye movement (REM) and slow wave sleep (SWS). Given that memory deficits are putative risk factors for depression and anxiety, we hypothesized that memory deficits might mediate the association between elevated high-frequency EEG activity and greater symptom severity. A sample of 149 healthy adults (ages 18-59) encoded scenes featuring either negative (e.g., snake) or neutral objects (e.g., chipmunk) placed on neutral backgrounds (e.g., forest). Participants indicated whether an object or a background was the same, similar or new compared to what they encountered during encoding. Participants also underwent one night of laboratory-monitored polysomnography to assess trait-level spectral bandpower. General distress (a broad underlying factor of negative affect common to both depression and anxiety) was assessed using questionnaires. Results indicated that elevated beta and gamma power during REM sleep were significantly associated with false memory for negative objects (i.e., mistakenly recognizing negative objects not presented during encoding), which was in turn linked to greater general distress. During SWS, higher beta power was associated with reduced overall memory accuracy across all scene components, which was in turn related to greater general distress. However, mediation effects were not significant after controlling for age and sex. These results suggest that memory impairments may serve as a pathway linking trait-like, hyperarousal-related physiological profiles during REM and SWS to the increased comorbidity of depression and anxiety.