Sleep spindle density and temporal clustering are associated with sleep-dependent memory consolidation in Parkinson's disease

Sleep is required for successful memory consolidation. Sleep spindles, bursts of oscillatory activity occurring during non-REM sleep, are known to be crucial for this process and, recently, it has been proposed that the temporal organization of spindles into clusters might additionally play a role in memory consolidation. In Parkinsons disease, spindle activity is reduced, and this reduction has been found to be predictive of cognitive decline. However, it remains unknown whether alterations in sleep spindles in Parkinsons disease are predictive of sleep-dependent cognitive processes like memory consolidation, leaving open questions about the possible mechanisms linking sleep and more general cognitive state in Parkinsons patients. The current study sought to fill this gap by recording overnight polysomnography and measuring overnight declarative memory consolidation in a sample of thirty-five Parkinsons patients. Memory consolidation was measured using a verbal paired-associates task administered before and after the night of recorded sleep. We found that lower sleep spindle density at frontal leads during non-REM stage 3 was associated with worse overnight declarative memory consolidation. We also found that patients who showed less temporal clustering of spindles exhibited worse declarative memory consolidation. These results suggest alterations to sleep spindles, which are known to be a consequence of Parkinsons disease, might represent a mechanism by which poor sleep leads to worse cognitive function in Parkinsons patients. Statement of significanceSleep -- particularly spindle activity -- is critical for memory consolidation, a core cognitive process. Changes to the architecture and oscillations of sleep are well documented in Parkinsons disease (PD) and have been associated with worse overall cognition. However, whether altered sleep plays a causal role in this relationship, by directly interfering with sleep-dependent cognitive processes, or whether it represents a mere epiphenomenon of advancing disease, remains unknown. Our study is the first to investigate a possible direct relationship between sleep and cognition in PD. We show that sleep spindles and their temporal clustering into trains relate to impairments in overnight declarative memory consolidation in patients. These findings are an important first step towards identifying modifiable sources of cognitive impairment in PD.