bluuebunny/crossref_metadata_2025_split huggingface dataset:
0237 Sleep Reactivity Prospectively Predicts Distress Reactions to the COVID-19 Pandemic 3-4 Years Later
Authors: Reffi Anthony , Cheng Philip , Kalmbach David , Sultan Zain , Drake Christopher 
Published: May 2022

Abstract

Introduction
The 2019 coronavirus disease (COVID-19) pandemic is a protracted stressor with far-reaching effects on daily life. Although most individuals exhibit resilience in the wake of adversity, it is not clear which characteristics reliably predict resilience versus longstanding distress. It is vital to delineate predictors of pandemic-related distress to highlight modifiable risk factors that can be targeted to enhance psychological resilience. Sleep reactivity may be an important predictor of pandemic reactions because it reflects a vulnerability to experience pronounced sleep disturbances in response to stress, which serve as barriers to healthy adjustment to adversity. Therefore, this study tested sleep reactivity as a prospective predictor of pandemic-related distress.

Methods
Participants were recruited from a previous randomized controlled trial (RCT) comparing self-guided digital CBT-I against a sleep education control in treating insomnia and preventing depression. Participants in the RCT were enrolled between 2016-2017 and were eligible for this follow-up study conducted between April and May 2020 (N = 208; dCBT-I: n = 102; control: n = 106). Pre-treatment sleep reactivity was measured in 2016-2017 (T1) using the Ford Insomnia Response to Stress Test (FIRST). COVID-19 distress was measured in April 2020 (T2) using the Impact of Events Scale (IES) and Quick Inventory of Depressive Symptomatology (QIDS). All analyses controlled for treatment condition and COVID-19 impact.

Results
T1 FIRST predicted T2 IES (b = 0.29, + 0.14 SE, p &lt; .05) and QIDS (b = 0.16, + 0.04 SE, p &lt; .001), such that higher sleep reactivity pre-pandemic predicted more severe stress responses and depressive symptoms during the pandemic 3-4 years later. Exploratory analyses revealed T1 FIRST was a predictor of the IES subscales arousal and intrusions (bs = 0.02, + 0.01 SEs, ps &lt; .05), but not avoidance.

Conclusion
These findings build on evidence that sleep reactivity prospectively predicts reactions to trauma and demonstrate its predictive utility generalizes to pandemic responses. Sleep reactivity is a modifiable risk factor that may be targeted using cognitive-behavioral or mindfulness-based approaches, and thus may offer a new pathway to resilience.

Support (If Any)
Support for P.C. was provided from the National Heart Lung and Blood Institute (K23HL138166).
0246 Sleep Hygiene Mediates The Relationship Between Depression And Sleep Quality In College Freshman
Authors: Hirsch Sophie , Zendels Philip , Peach Hannah , Gaultney Jane 
Published: May 2022

Abstract

Introduction
A variety of attitudes, behaviors, and health attributes can influence sleep quality. Depression and sleep quality interact bidirectionally, with depressed individuals often sleeping worse. College freshman may be prone to worse sleep and depression due to significant lifestyle changes, including sleep hygiene (a set of behaviors and conditions promoting sleep). This study sought to examine the relationship between sleep hygiene and depression in predicting sleep quality in first-year college students.

Methods
165 participants were recruited to investigate sleep behaviors associated with stress, mental health, physical activity and eating as they entered college. Data were recorded using the Pittsburgh Sleep Quality Index (PSQI; Buysse et al., 1989), the Sleep Hygiene Practice Scale (SHPS; Lin et al., 2007; Yang et al., 2010) and the Center for Epidemiological Studies-Depression (CESD; Radloff, 1977). A simple mediation analysis was run using the PROCESS macro for SPSS (Model 4; Hayes, 2018) with age and gender as covariates to examine direct and indirect associations of depression on sleep quality via sleep hygiene practices.

Results
In the model predicting sleep hygiene (R2 = .33, p &lt; .001), depression had a significant effect (b = 1.90, p &lt; .001), suggesting individuals scoring higher for depression engaged in more unhealthy sleep hygiene behaviors. The model predicting sleep quality (R2 = .47, p &lt; .001) had significant effects from depression (b = .11, p = .005) and sleep hygiene (b = .09, p &lt; .001) suggesting both higher depression scores and poor sleep hygiene behaviors associate with worse sleep quality. The indirect pathway was also significant (b = .17, CI: .11 - .24), suggesting depression’s impact on sleep hygiene behaviors also contributes to sleep quality.

Conclusion
One connection between depression and reduced sleep quality may be indirect via maladaptive sleep hygiene. Future research should look at addressing mental health with incoming students and promoting healthy lifestyle behaviors.

Support (If Any)
NA
0252 Sleep Hygiene Education Intervention: Psychological and Physiological Associations with Sleep in College Students
Authors: Horton Alexis , Gibson Matelyn , Anderson Noah , Mullins Kayla , Reynolds Alexandria 
Published: May 2022

Abstract

Introduction
College students tend to struggle with managing healthy sleep habits; these unhealthy behaviors can lead to poor sleep and impact their overall mental and physical health. More specifically, sleep is intimately connected to psychological and physiological factors such as anxiety, depression, and blood pressure. The focus of the current study was to examine habitual sleep habits in college students, provide a brief educational intervention, and investigate potential changes in psychological and physiological health.

Methods
Participants included 14 undergraduate students (6 men, average age M=20.64 years, SD=2.13) who wore wrist actigraphs to measure their typical sleep habits. After one week, participants completed questionnaires about sleep (Pittsburgh Sleep Quality Index, PSQI), sleepiness (Epworth Sleepiness Scale, ESS), fatigue (Multidimensional Assessment of Fatigue Scale, MAF), and psychological symptoms (i.e., depression, anxiety, and stress; Depression Anxiety Stress Scales, DASS-21). Blood pressure and heart rate were measured using a wrist device. Subjects participated in a short lecture about healthy sleep hygiene habits and the importance of sleep and then repeated the one-week observational study.

Results
Paired sample t-tests revealed a significant increase from baseline average sleep duration (M=5.83 hours) to post-intervention sleep duration (6.64 hours; t(13)=-2.532, p=.013). Sleep efficiency (actigraphy) and quality (PSQI) did not improve significantly. ESS scores decreased significantly (t(13)=3.76, p=.002 (pre M=9.29; post M=5.43) and MAF scores decreased significantly (t(13)=2.19, p=.047 (pre M=20.48; post M=15.60). No significant differences were found in depressive, anxiety, or stress symptoms when comparing DASS-21 scores pre- vs post-intervention. Baseline systolic blood pressure (M=114.88) significantly decreased compared to post-intervention recordings (M=108.21). Diastolic blood pressure and heart rate did not differ significantly.

Conclusion
The results of this study suggest that one educational lecture about sleep hygiene may be a start to improving sleep in college students. Even a 48-minute increase resulted in decreased sleepiness and fatigue. However, no improvements were found in sleep quality or efficiency. Although a slight improvement was found in systolic blood pressure, no other physiological or psychological benefits were noted. More research should be conducted on how to improve sleep habits in college students beyond an educational approach.

Support (If Any)
None.
0266 Sleep Spindle-Duration: A Potential Biomarker for Neurodegenerative Disorder Phenotyping
Authors: Levendowski Daniel , Walsh Christine , Boeve Bradley , Tsuang Debby , Salat David , Hamilton Joanne , Shprecher David , Lee-Iannotti Joyce , Westbrook Philip , Berka Chris , Mazeika Gandis , Neylan Thomas , Louis Erik St 
Published: May 2022

Abstract

Introduction
Decreased sleep spindle oscillations were previously associated with cognitive decline in older adults, increased tau levels, and phenoconversion to dementia in patients with Parkinson disease (PD). We analyzed quantitative sleep spindle measures to determine if this biomarker was associated with particular neurodegenerative disorder syndromes.

Methods
Sleep spindle oscillations ascertained in patients broadly characterized as presumed Parkinsonian-spectrum disorders (PSD), which included the subtypes dementia with Lewy Bodies/Parkinson Disease Dementia (DLB/PDD, n=16), PD (n=16), isolated REM sleep behavior disorder (iRBD, n=19), and progressive supranuclear palsy (PSP, n=13), were compared with non-PSD subtypes Alzheimer Disease dementia (AD, n=22), mild cognitive impairment (MCI, n=35), and normal cognition (NC, n=61). Sleep Profiler studies were conducted in all participants. The automated spindle detection algorithms recognized temporal excursions in the alpha (8-12 Hz) and sigma (12-16 Hz) power of 250 milliseconds or greater, with spindle duration being the sum of all spindle elapsed times. Night-to-night variability was assessed in PSP=13, PD=16, DLB/PDD=12, AD=17, MCI=25, and NC=53. Statistical analyses included intraclass correlations (ICC) and Bland-Altman plots for two-night data, and Mann-Whitney U-tests and multiple logistic regression applied to sleep-time weight-averaged spindle-durations.

Results
The night-to-night spindle-duration ICC was 0.95 (P&lt;0.0001), with a Bland-Altman bias of 0.05+/-2.83 minutes. Spindle-duration was independently associated with PSD versus non-PSD groups (P=0.017, OR 1.08, 95%-CI 1.01-1.15), but not significantly associated with age (P=0.12, OR 1.03, 95%-CI 0.99-1.07) or sex (P=0.54). When stratified by subtype, age was associated with spindle-duration when NC were compared to AD and MCI (P=0.0003, OR 1.10, 95%-CI 1.04-1.16) and when iRBD were compared to DLB/PDD, PD and PSP (P&lt;0.05, OR 1.00, 95%-CI 0.89-1.13)Spindle-durations were reduced in PSP (0.9+/-2.1) and DLB/PDD (2.0+/-5.1) when individually compared to AD (3.2+/-7.1), iRBD (3.3+/-3.4), PD (5.3+/-6.6), MCI (5.3+/-9.7), and NC (8.0+/-11.1) subtypes (all P&lt;0.05). AD patients also exhibited lower spindle-durations than NC (P=0.03).

Conclusion
Auto-detected sleep spindle-durations exhibited excellent night-to-night reliability in both NC and patients with neurologic disorders. Decreased sleep spindle-duration was independently associated with PSP and DLB/PDD, and in AD. Reduced sleep spindle duration may be a distinct sleep biomarker for those disorders likely indicating thalamocortical dysfunction.

Support (If Any)
NIA grants: R44AG050326, R44AG054256, P30AG62677 and R34AG56639.
0271 Actigraphy Based Measures of Sleep Disruption and Circadian Rhythms in the WashU Biomarkers of Alzheimer’s Disease in Sleep and EEG (BASE) Cohort
Authors: Milman Noah , Madden Katherine , Reynolds Christina , Balba Nadir , Omar Tanya , Lim Miranda , Ju Yo-El 
Published: May 2022

Abstract

Introduction
Prospective studies of Alzheimer’s disease (AD) demonstrate sleep-wake disturbances may precede and accelerate with cognitive decline. Use of wrist-actigraphy in conjunction with overnight polysomnography (PSG) enables researchers to evaluate diverse characteristics of sleep and circadian rhythms. Though outcome measures from these devices have been implicated in the progression of AD, because of great individual differences, it is valuable to internally replicate within cohort. Here we demonstrate application of actigraphy in the context of healthy aging to identify patterns of activity that predict cognitive decline.

Methods
Participants were prospectively recruited at Washington University as part of the BASE study and wore an Actiwatch2 (Philips-Respironics) and cross-validated for sleep and wake using polysomnography. The watch was worn continuously for at least 5 consecutive nights to be included in the analysis (n = 68, age = 71.1 ± 4.5 years). Rest-activity rhythms were computed using compiled code from National Sleep Research Resource (actiCircadian) pipeline implemented in MATLAB R2021a (Mathworks). Clinical Dementia Rating (CDR) scales and cognitive tests were conducted on the first day of actigraphy recording.

Results
Individuals with cognitive impairment (CDR Global Score &gt; 0) had increased wake after sleep onset (WASO) and reduced sleep efficiency compared with individuals with no impairment (CDR = 0). (unpaired ttest: p = 0.02 and p = 0.02). Participants with cognitive impairment had a trend toward reduced relative amplitude (RA) (p = 0.06). Reduced (worse) RA was correlated with worse performance on the Trail Making Task A (Pearson r: -0.37, p = 0.002). Higher (better) interdaily Stability (IS) was associated with better responses on subjective questionnaires including Epworth Sleepiness Scale and Pittsburgh Sleep Quality Index (Pearson r: -0.24 p = 0.051; r: 0.242, p = 0.047, respectively).

Conclusion
Actigraphically-derived rest-activity metrics are correlated with cognitive status, cognitive test performance, and subjective sleep questionnaires.

Support (If Any)
NIH R01 AG059507, ARCS Foundation Scholar
0276 Sleep EEG Changes in a Transgenic Mouse Model of Spinocerebellar Ataxia Type 3
Authors: Tsimpanouli Maria-Efstratia , Ghimire Anjesh , Barget Anna , Weston Ridge , Costa Maria do Carmo , Watson Brendon 
Published: May 2022

Abstract

Introduction
Spinocerebellar ataxia type 3 (SCA3) or Machado-Joseph disease is a fatal, incurable, dominantly inherited ataxia, typically of adult-onset, and the most frequent type of SCA worldwide. SCA3 patients show progressive neuronal loss in several brain areas reflecting a broad spectrum of motor and non-motor symptoms, including ataxia, parkinsonism, and sleep disorders. In other neurodegenerative diseases, sleep disturbances alter brain homeostatic mechanisms, including DNA repair, synaptic function, and network activity, leading to deterioration of neurologic function. Sleep research has provided insights into their pathophysiology, disease prediction, and symptom management. Such studies have not been performed in SCA3. The aim of this study is to characterize sleep EEG in an SCA3 transgenic mouse model.

Methods
We used homozygous, hemizygous, and wild-type YACMJD84.2 littermate mice. To confirm the expected disease phenotype, we assessed for locomotor and exploratory activity in the morning and evening when the mice were 22 to 31 weeks old. We then implanted 6 electrodes in the frontal, parietal, and cerebellar areas. About two weeks after, we recorded their sleep activity for 15 hours (ZT0-15) per day for three consecutive days. We analyzed the data from the open-field testing and the EEG from the third day of recordings using SPSS and Matlab and a p&lt;0.05 was considered for statistical significance.

Results
As expected, homozygous SCA3 mice showed statistically significant decreased locomotor and exploratory activities compared with wild-type littermates. In terms of sleep architecture we did not observe any significant differences between the different genotypes. Moreover, compared with wild-type, homozygous SCA3 mice displayed increased β spectral power band activity during REM. They also had decreased θ band activity, β band activity, spindle activity, and γ band acitivity during wake.

Conclusion
Our data suggest that EEG spectral power is dysregulated in homozygous SCA3 mice. Changes in β band have been observed in SCA3 patients during wake, and in patients with REM sleep behavior disorder. Therefore, future studies analyzing the sleep EEG of SCA3 patients are needed to confirm whether our findings are translatable. Further studies should also investigate the causal relationship between the observed differences in sleep and disease progression. Gaining greater insight into the role of sleep in SCA3 could provide translatable biomarkers and lead to improved assessment of the disease progression and therapeutic interventions.

Support (If Any)
NHLBI 5T32HL110952
0281 Impact of chronic sleep disruption on glymphatic function, cognitive performance, and neuropathology in the 5xFAD mouse model
Authors: Pedersen Taylor , Keil Samantha , Agarwal Sanjana , Badran Mohammad , Gozal David , Iliff Jeffrey 
Published: May 2022

Abstract

Introduction
Recent studies suggest a bidirectional relationship between sleep disruption and Alzheimer’s disease, with mid-life sleep disruption associated with the development of Alzheimer’s-related amyloid and tau pathology. Yet, the mechanistic link between sleep disruption, particularly over chronic time scales, and the development of Alzheimer’s pathology remains unclear.

Methods
In this study, we evaluated the impact chronic sleep disruption has on the onset of cognitive impairment and neuropathologic disease progression using the 5xFAD amyloidosis mouse model. Chronic sleep disruption in male and female C57BL/6 and 5xFAD+ mice was performed in Lafayette sleep fragmentation cages from 10-18 weeks of age. Cognitive impairment was evaluated through behavioral tasks indicative of spatial memory, short-term memory, locomotion, anxiety, and activities of daily living. Upon completion of behavioral experiments, glymphatic function was assessed by measuring the influx of fluorescent cerebrospinal fluid tracers into brain tissue. Aquaporin-4 localization, amyloid plaque deposition, and markers of astroglial and microglial activation were assessed by immunofluorescence.

Results
We observed that chronic sleep disruption impaired cognitive performance and increased neuropathological outcomes in 5xFAD+ and littermate controls. The impact on glymphatic function was assessed in parallel and correlated with neuropathological and behavioral outcomes.

Conclusion
These findings highlight the critical association between dysfunctional sleep and the development of cognitive impairment and neuropathologic disease progression. They indicate that there is a potential interaction between inflammatory expression after chronic sleep disruption and neuropathologic disease progression.

Support (If Any)
0300 Early Life Sleep Fragmentation Impairs Hippocampal-Dependent Learning and Sleep-Dependency in Hippocampal Calcium Transients
Authors: Zamore Zachary , Chou Allison Tzu-Han , Schifman Naomi , Fenik Polina , Pullum Keelee , Slinger Michelle , Veasey Sigrid 
Published: May 2022

Abstract

Introduction
Sleep deprivation impairs hippocampal-dependent memory, and hippocampal-dependent memory impairments occur in some dementias, including Alzheimer’s disease. As our population continues to age, understanding the molecular basis for memory impairments is increasingly important. We hypothesized that early life sleep fragmentation would result in lasting increases in hippocampal calcium transient activity.

Methods
B6 mice were randomized to 12wk of sleep fragmentation or rested control conditions at age 8wk. Mice were microinjected with AAV9-CamKII-GCamp6F into the hippocampus and later implanted with a GRIN Lens into CA1 secured to a baseplate along with chronic EEG/EMG electrodes and recording connector. Calcium recordings were obtained two to three months after injection and recordings were obtained across sleep-wake cycles&gt;4mins of wake and NREM sleep. Individual cells across animal were combined into sleep fragmented (n = 521 cells) or rested (n = 443 cells) groups during wake or sleep. Average FFx was analyzed by group and condition by T-tests, paired for within and unpaired across groups. A spatial object recognition assay was also performed on all mice (n=16 for both groups) and performance across group was analyzed by paired T-tests.

Results
Rested mice showed normal spatial object recognition (n = 16, p&lt;0.05). In contrast, SF mice showed impaired spatial object recognition (n = 16, N.S.). There were no differences across sleep conditions in calcium transient FFx for waking (p&gt;0.05). However, in sleep, cells in SF mice had significantly higher average FFx values than cells in rested mice (p&lt;0.0001).

Conclusion
Early-life sleep fragmentation has long-lasting impacts on memory. Since spatial memory is dependent on hippocampal function, the calcium transient FFx data suggests that a driver of this hippocampal memory impairment may be higher firing rates in sleep and/or greater calcium exposure in hippocampal CamKII neurons in sleep, both of which may perturb microglial maintenance of synapses. Understanding the molecular drivers behind this calcium dysfunction will be essential in our understanding of neurodegeneration, dementia, and Alzheimer’s disease.

Support (If Any)
NIH AG054104; AG064231
0303 The Effects of Latitude on Sleep at 4300m
Authors: Wehling Richard , Jung Christopher 
Published: May 2022

Abstract

Introduction
Worldwide, 140-million people live above 2400m and even more visit high altitudes (HA) annually. Exposure to HA is associated with hypoxia-related cognitive impairments and sleep disruptions. Additionally, both planetary axial tilt, solar gravity, and planetary spin distort the earth’s atmosphere pulling the equator’s atmosphere further from the earth’s surface when compared to the poles. These forces may have additional impacts on physiology at HA. There has yet to be a study to determine these effects of latitude on physiology at HA. Therefore, the aim of the current study was to determine if latitude exacerbates the effects of HA on sleep.

Methods
Similar testing protocols were utilized at 4,300m at Camp-14 on Denali at a latitude of ~63° and in the village of Dingboche on the route to Mount Everest at a latitude of ~28°. Exclusion criteria included 18-65 years, self-reported drug use, cigarette-smoking, sleep disorders, abnormal body mass index (BMI), falling asleep more than one hour or awakened more than an hour during the night. Wireless sleep recording devices recorded the sleep architecture of qualified participants. Twenty-two climbers (3 females) participated in the Denali study (age 34.0±9.7 mean±SD) and twenty-five climbers (6 females) participated in the Everest study (age 28.0±9.7 mean±SD). Participants were instructed to go to bed and wake up at their habitual bedtimes and wake times.

Results
Independent t-tests revealed a statistically significant decrease in total sleep (p&lt;0.05) on Denali when compared to Mt. Everest. There were nonsignificant trends for a decrease in rapid eye movement (REM) and sleep onset latency on Denali. Other sleep stages appear relatively unaffected by latitude.

Conclusion
Our findings indicate that a decrease in total sleep time occurs at higher latitude with comparable altitude. Prior research has linked a decrease in total sleep time to decreased cognitive impairments and physiologic disruptions. Our findings suggest that latitude should be considered when venturing into HA environments, designing research protocols, analyzing results, and clinical applications or military operations.

Support (If Any)