Abstract

AbstractBackgroundSleep has been identified as a modifiable factor involved in both the development and progression of Alzheimer’s disease (AD). Previous findings have suggested that poor sleep may be associated with increased risk of AD. Conversely, higher quality of sleep may slow progression of pathophysiological mechanisms in mild cognitive impairment (MCI) through functional connectivity reorganization of neural networks underlying higher cognitive functions.MethodIn clinic, 38 MCI patients and 38 age‐matched controls completed structural magnetic resonance imaging (MRI), resting‐state functional MRI (rs‐fMRI), and a cognitive test battery, covering memory, executive functions, and language. The Sleep Continuity in Alzheimer’s Disease Scale (SCADS) was used to assess sleep quality. Patients were stratified into “good” (n=20) and “poor” (n=18) sleepers, using the median SCADS score as a cut‐point. Default mode (DMN) and left and right frontoparietal (FPN) networks were reconstructed through an independent component analysis approach. Differences in network connectivity across MCI groups were investigated with non‐parametric inference using FSL randomize (n=5000 permutations), corrected at a threshold‐free‐cluster enhancement level of pFWE < 0.025. Grey matter and sex were inserted as covariates in the analysis. The same model was implemented to investigate associations between connectivity and cognition in MCI. Finally, between‐network connectivity was assessed through partial correlation with sex as covariate.ResultMCI good sleepers showed increased FPN connectivity compared to MCI poor sleepers. Increased FPN connectivity was positively associated with language performance in the former group. Finally, we found a positive coupling connectivity between DMN and FPN and between left and right FPN in MCI good sleepers, while this pattern was disrupted in MCI patients with lower quality of sleep.ConclusionThese findings suggest a relationship between sleep quality and FPN connectivity in MCI, highlighting possible sleep‐induced compensatory mechanisms. Future studies in larger samples using longitudinal methods and objective measures of sleep will be necessary to confirm this finding. However, these results further support the concept that better sleep may be protective on the pathway to AD.

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