A growing body of evidence suggests that sleep can help to decouple the memory of emotional experiences from their associated affective charge. This process is thought to rely on the spontaneous reactivation of emotional memories during sleep, though it is still unclear which sleep stage is optimal for such reactivation. We examined this question by explicitly manipulating memory reactivation in both rapid-eye movement sleep (REM) and slow-wave sleep (SWS) using targeted memory reactivation (TMR) and testing the impact of this manipulation on habituation of subjective arousal responses across a night. Our results show that TMR during REM, but not SWS significantly decreased subjective arousal, and this effect is driven by the more negative stimuli. These results support one aspect of the sleep to forget, sleep to remember (SFSR) hypothesis which proposes that emotional memory reactivation during REM sleep underlies sleep-dependent habituation.

Of 4692 studies identified, 60 were retained (28 adult, 32 pediatric). Most studies included diet patterns, quality, or energy intake as confounders, while a few examined these dietary variables as mediators or effect modifiers. There was some evidence, mostly in pediatric studies, that inclusion of diet altered sleep-cardiometabolic health associations. Diet plays a diverse role within sleep-cardiometabolic health associations. Investigators should carefully consider the conceptualization of diet variables in these relationships and utilize contemporary statistical approaches when applicable.

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Spinocerebellar ataxia type 3 (SCA3) is a neurodegenerative disorder showing progressive neuronal loss in several brain areas and a broad spectrum of motor and non-motor symptoms, including ataxia and altered sleep. While sleep disturbances are known to play pathophysiologic roles in other neurodegenerative disorders, their impact on SCA3 is unknown. Using spectrographic measurements, we sought to quantitatively characterize sleep electroencephalography (EEG) in SCA3 transgenic mice with confirmed disease phenotype. We first measured motor phenotypes in 18–31-week-old homozygous SCA3 YACMJD84.2 mice and non-transgenic wild-type littermate mice during lights-on and lights-off periods. We next implanted electrodes to obtain 12-h (zeitgeber time 0-12) EEG recordings for three consecutive days when the mice were 26–36 weeks old. EEG-based spectroscopy showed that compared to wild-type littermates, SCA3 homozygous mice display: (i) increased duration of rapid-eye movement sleep (REM) and fragmentation in all sleep and wake states; (ii) higher beta power oscillations during REM and non-REM (NREM); and (iii) additional spectral power band alterations during REM and wake. Our data show that sleep architecture and EEG spectral power are dysregulated in homozygous SCA3 mice, indicating that common sleep-related etiologic factors may underlie mouse and human SCA3 phenotypes.

Introduction Sleep-disordered breathing (SDB) is a common sleep disturbance and is associated with both incident and recurrent cardiovascular disease (CVD). Respiratory Cycle-Related EEG Changes (RCREC), an SDB biomarker, are thought to reflect inspiratory microarousals and are based on quantitative analysis of sleep EEG and breathing. The objective of this study was to assess whether RCREC may predict CVD incidence or recurrence in a large cohort of adults. The RCREC for several frequency bands have been previously shown to predict either higher or lower all-cause mortality in the same cohort. Methods Data were obtained from the Sleep Heart Health Study (SHHS), a multicenter longitudinal study that included polysomnograms in middle-aged to older adults. Information about CVD events was collected at baseline and for up to 16 years later. The RCREC values at baseline were computed in the delta, theta, alpha, sigma, beta, and gamma frequency bands during scored epochs of sleep. Cox Proportional Hazard models, were used to assess the relation of each RCREC frequency band and incidence or recurrence of CVD. These models were stratified by sex and adjusted for body-mass index, age, race, smoking status, diabetic status, hypertensive status, HDL cholesterol, LDL cholesterol, and the apnea-hypopnea index (AHI). Results There were 3,032 adults with sufficient data quality (mean age at baseline 62±11(SD) years, 58% female). Among 2,500 adults with no reported prior CVD history at baseline, the adjusted odds ratios (95% CI) for delta RCREC 0.948(0.920–0.977), theta RCREC 0.938(0.895–0.984), and alpha RCREC 0.946(0.902–0.993) separately suggested associations with lower CVD incidence, whereas gamma RCREC 1.017(1.001–1.032) predicted a marginal increase. Among 532 adults having prior CVD history at baseline, delta RCREC 0.958(0.927–0.989) and sigma RCREC 0.931(0.895–0.969) separately predicted decreased CVD recurrence. The apnea-hypopnea index (AHI) was not similarly predictive in any model. Conclusion The RCREC for several frequency bands, in contrast to AHI, may predict CVD incidence and recurrence. The directionality of the association was surprising and merits further exploration. Support NIH:NCATS-TL1-TR-002242, BD2K-K01-ES-026839, HL105999