Abstract
Recent evidence showed that EEG activity alterations that occur during sleep are associated with structural, age-related, changes in healthy aging brains, and predict age-related decline in memory performance. Alzheimer’s disease (AD) patients show specific EEG alterations during sleep associated with cognitive decline, including reduced sleep spindles during NREM sleep and EEG slowing during REM sleep. We investigated the relationship between these EEG sleep alterations and brain structure changes in a study of 23 AD patients who underwent polysomnographic recording of their undisturbed sleep and 1.5T MRI scans. Cortical thickness measures were correlated with EEG power in the sigma band during NREM sleep and with delta- and beta-power during REM sleep. Thinning in the right precuneus correlated with all the EEG indexes considered in this study. Frontal–central NREM sigma power showed an inverse correlation with thinning of the left entorhinal cortex. Increased delta activity at the frontopolar and temporal regions was significantly associated with atrophy in some temporal, parietal, and frontal cortices, and with mean thickness of the right hemisphere. Our findings revealed an association between sleep EEG alterations and the changes to AD patients’ brain structures. Findings also highlight possible compensatory processes involving the sources of frontal–central sleep spindles.
Highlights
In recent years, the research on Alzheimer’s disease (AD) has seen growing interest in the alterations of sleep physiology and their possible role in the progression of the disease
Delta activity, occurring at temporo-parieto-occipital regions during rapid eye movement sleep (REM) sleep, has been shown to correlate with the integrity of frontal and prefrontal regions [24]. These findings support the idea that structural brain changes can alter EEG activity during sleep and impair some of the critical functions that sleep performs in daily life. Moving from this evidence, we investigated the relationship between cortical thickness, measured using magnetic resonance imaging (MRI), and the major EEG alterations during non-rapid eye movement sleep (NREM) and REM sleep in AD patients [19], i.e., sigma EEG power during NREM sleep reflecting impaired spindle activity, and delta and beta power during REM sleep as indexes of the EEG slowing phenomenon
Delta activity at frontotemporal regions during REM sleep is significantly correlated to the mean thickness of the right hemisphere and, might be considered an EEG index of the neurodegenerative process in brains affected by AD
Summary
The research on Alzheimer’s disease (AD) has seen growing interest in the alterations of sleep physiology and their possible role in the progression of the disease. Sleep seems to be a privileged physiological state for beta-amyloid clearance [1,2], while waking hours are characterized by progressive beta-amyloid deposition as a function of the time spent awake [3,4,5]. Some quantitative EEG studies have described the alterations of cortical activity observed in sleeping AD patients. Sleep spindles are phasic phenomena characteristic of NREM sleep, generated in the thalamo-cortical system [11]. These fast phasic oscillations are involved in sleep-dependent memory consolidation processes and in the corticalization of hippocampus-dependent memory traces [15]. Sleep spindle density is correlated with sleep-dependent gain in declarative memory performance in both healthy aging [16] and AD-related cognitive impairment [12]
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