Slow waves contribute to memory consolidation only in older adults without sleep‐disordered breathing

Abstract

Background Sleep‐dependent memory consolidation, which is thought to rely on the dialogue between the hippocampus and the medial prefrontal cortex (mPFC) during NREM sleep, is mediated by slow waves (SW) and sleep spindles. Some studies indicate that this process is impaired in ageing but also in sleep‐disordered breathing (SDB), a very common sleep disorder in ageing. In this study, we investigated sleep‐dependent memory consolidation in older adults with or without SDB and explored the underlying mechanisms. Method Baseline data of 57 cognitively unimpaired older adults (mean age ± SD: 68.6 ± 3.3 years) from the Age‐Well cohort were analysed. Participants underwent a structural MRI scan to obtain mPFC and hippocampal grey matter volumes, and performed a visuospatial memory task until reaching a learning criterion of 66.6% of correct answers. Post‐learning sleep was monitored using polysomnography, and delayed recall was probed the next morning. An overnight change in memory performance (OCMP) was computed as follows: (recall performance – learning performance) / learning performance. SW, slow and fast spindles during N2 and N3 sleep were automatically detected using the SleepTrip toolbox. Based on the standard apnea‐hypopnea index (AHI) cutoff of 15 events/h, participants were classified as having SDB (SDB+, n=47) or not (SDB‐, n=10). Result There was no between‐group difference in OCMP, as well as in amplitude, duration and frequency of SW, slow and fast spindles (p>0.05). However, we found a significant group by SW density interaction after controlling for age, sex, education, total sleep time and trait‐anxiety (p=0.03). Thus, a positive association was only found between SW density and OCMP in the SDB‐ group (p=0.02; Fig 1). No correlation was found between slow or fast spindle density and OCMP in either group. Finally, mPFC and hippocampal volumes did not differ between SDB+ and SDB‐ participants (p>0.05), but SW density positively correlated with the volume of the mPFC (p=0.01; Fig 2). Conclusion Our findings suggest that the contribution of SW to sleep‐dependent memory consolidation is impaired in participants with SDB and incriminate the mPFC. We plan to conduct connectivity and SW‐spindle coupling analyses to unravel the functional substrates of this deficit.