Sleep fragmentation (SF) increases with age, and is related to both cognitive impairment and increased risk of developing dementia. The mechanisms underlying these relationships are still unclear, but emerging evidence suggests that non-rapid eye movement (NREM) sleep may play a role in clearing β-amyloid (Aβ) from the brain. Thus, a disruption of NREM-sleep could exacerbate Aβ deposition. Our objective was to investigate the relationships between NREM-SF and brain structure, metabolism and amyloid deposition as well as cognitive performance in elders.
31 cognitively normal older adults (mean age ± SD: 72.2 ± 6.9 years) underwent a detailed neuropsychological assessment and structural MRI, FDG-PET and florbetapir-PET scans to assess grey matter (GM) volume, brain glucose metabolism, and amyloid deposition respectively. Sleep-wake activity was recorded during 7 consecutive nights using actigraphy (MotionWatch8, CamNtech). The mean level and night-to-night SF variability were computed over the first half of the night. Voxelwise multiple regression analyses were performed between SF parameters and neuroimaging data using SPM12, controlling for age and the other SF parameter (i.e. variability when the mean level was considered, and conversely).
The mean level of NREM-SF negatively correlated to brain glucose metabolism within the ventromedial prefrontal cortex (vmPFC), hippocampus, and insula (p<0.001, Figure 1a), and was associated to lower cognitive performance, notably in executive functioning and episodic memory (p<0.05). Variability of NREM-SF negatively correlated to vmPFC GM volume (p<0.005, Figure 1b) and positively correlated to amyloid burden in the same region (p<0.001, Figure 1c).
In the present study, we showed a negative impact of high intensity and variability of NREM-SF on cerebral structure, function and Aβ deposition. These effects were found in the vmPFC known to be sensitive to ageing and amyloid deposition, as well as the hippocampus, a key structure of episodic memory processes. SF was also associated to reduced cognitive performances, highlighting the importance of sleep continuity to brain and cognition maintenance in ageing. Further investigations are now needed to determine whether interventions aiming at improving sleep quality might reduce age-related cognitive and brain alterations.