bluuebunny/crossref_metadata_2025_split huggingface dataset:
0039 An Apple a Day Keeps Bad Sleep Away? Carotenoid Consumption and Multimodal Sleep Outcomes in Adolescents
Authors: Kamhout Sarah , Duraccio Kara 
Published: April 2024

Abstract

Introduction
Carotenoid consumption has been linked with greater likelihood of appropriate sleep duration and higher levels of sleep quality in adults. As only 2-7% of American adolescents met recommended fruit and vegetable intake guidelines in 2017, and over 70% of high schoolers regularly sleep less than 8 hours per night, adolescents may be especially influenced by relationships between poor diet and poor sleep. Previous studies in this area have been limited to other age groups or examination of singular sleep constructs.

Methods
Seventy-four adolescents (14-18 years; 43 female) completed 2-3 ASA-24 dietary recalls across randomized weekend and weekdays. They also completed the Pittsburgh Sleep Quality Index (PSQI), the Epworth Sleepiness Scale for Children and Adolescents (ESS-CHAD), and a Dim-Light Melatonin Onset (DLMO) appointment. Bivariate regressions examined potential associations between average carotenoid consumption (α Carotene, β Carotene, β Cryptoxanthin, Lycopene, Leutin + Zeaxanthin) and self-reported sleep duration (PSQI Item 4), daytime sleepiness (ESS-CHAD Total) and melatonin onset time (DLMO, threshold 4 pg/mL). Subject age and sex were controlled for within each model. To correct for multiple comparisons, p was set to a significance threshold of 0.01 for predictors within the model and 0.05 for the entire model.

Results: Results
β Cryptoxanthin was a significant predictor of daytime sleepiness (beta=-.024, t(72)=-2.682, p=.009) and explained significant variance in the comprehensive model for this outcome (R2 = .072, F(3, 69)=2.901, p=.041). No other carotenoids emerged as significant predictors of sleep outcomes after correction for multiple comparisons. β Carotene neared significance for predicting duration (beta=-.258 , t(72)=-2.22, p=.030; R2 = .033, F(3, 69)=1.829, p=.15), as did Lycopene (beta=.243 , t(72)=2.086, p=.041; R2 = .026, F(3, 69)=1.632, p=.19).

Conclusion
β Cryptoxanthin could be investigated as a potential influence on daytime sleepiness in this age group. Further studies are needed to establish causality and to examine the clinical significance of consumption increases in this age group. Underconsumption of whole foods common to this developmental period may make it difficult to detect the effects of adequate or increased intake cross-sectionally.

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0042 Melanopsin Crispants in Zebrafish Display Difference in Sleep Latency
Authors: Doldur-Balli Fusun , Smieszek Sandra , Veatch Olivia , Keenan Brendan , Zimmerman Amber , Polymeropoulos Christos , Birznieks Gunther , Polymeropoulos Mihael 
Published: April 2024

Abstract

Introduction
Melanopsin (OPN4) is a blue light sensitive opsin type G protein couple receptor. It is highly expressed in the photsenstive ganglion cells which mediate responses to light including regulation of sleep, circadian photoentrainment and pupillary light responses. Mutations in OPN4 were shown to affect responses to light ultimately affecting the regulation of circadian rhythms and sleep patterns. Sleep homeostasis was altered in homozygous knockout of Opn4, gene encoding for melanopsin, in mice. Human melanopsin variants which alter function significantly may contribute to sleep disturbance, circadian dysfunction and visual impairment. In order to further dissect the role of melanopsin in sleep in a diurnal vertebrate model, we created an F0 knockout model of opn4 gene in zebrafish and assessed sleep/wake phenotype.

Methods
In CRISPR/Cas9 screening, single cell-stage zebrafish embryos were injected with injection cocktail containing Cas9 protein and crRNAs targeting opn4a and opn4b, homologous genes of human OPN4. Control groups were negative control crRNA injected embryos. Zebrafish larvae were individually pipetted into each well of a 96 well plate. Larval zebrafish were raised on a 14 hour/10 hour light/dark cycle at 28.5◻C until sleep phenotyping starts. Sleep phenotyping was carried out between days 5-8 post injection.

Results
Longer sleep latency at night was observed in opn4 CRISPR knockout larvae. This is in line with prior literature. Additional tests by exposing opn4 crispants and control zebrafish larvae to white light and dark pulses at different times were performed however the activity and sleep latency did not change across groups.

Conclusion
Sleep/wake phenotyping of opn4 (melanopsin) crispants in zebrafish displayed significant difference in sleep latency parameter compared to controls. Although additional tests carried out using pulses of white light need to be repeated, current results highlight the importance of OPN4 mediated pathways in affecting sleep latency.

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0048 Investigating the Effects of Consecutive Nights of Pre-sleep Alcohol Use on Sleep Spindle Density and Distribution
Authors: McCullar Katie , Barker David , McGeary John , Gredvig-Ardito Caroline , Saletin Jared , Carskadon Mary 
Published: April 2024

Abstract

Introduction
We previously reported the impact of consecutive nights of alcohol on sleep macrostructure variables. Sleep spindle density and distribution, however, remain unexamined in response to alcohol. This report tests the hypothesis that sleep spindle density will be lower following pre-sleep alcohol and most affected early in the sleep period.

Methods
Thirty (15F; ages=22-57, mean=33) healthy adult participants took part in a crossover, within-subjects study with two 3-night in-lab conditions: a Mixer + Alcohol condition targeted a BrAC of 0.08 mg/L and a counter-balanced Mixer-only condition; conditions were separated by ≥ 3 days. All drinking ended 1 hour before lights out. Sleep EEG derivations C3-A2 and C4-A1 were submitted to a validated sleep spindle detection algorithm (Ferrarelli, et al., 2007). Sleep spindle density in NREM sleep (#/min; Stages 2-4) was averaged between channels and submitted to a series of linear mixed-effects models. A first, 2x3 model examined the factors beverage and night (Nights 1-3) on NREM spindle density. Next, data were stratified into thirds of the night, with the model repeated for each third.

Results
A main effect of alcohol on sleep spindle density across the whole night was identified (F(1,145)=5.33, p=.022). Sleep spindle density was lower on Mixer + Alcohol nights (1.6±0.7 spindles/min) vs Mixer-only (1.9±0.5 spindles/min). No effect of Night(1-3) or interaction of beverage and night was observed (p’s&gt;.05). Next, we identified opposing effects of alcohol on sleep spindle density in early vs. late sleep. In the first third of the night sleep spindle density was lower on Mixer + Alcohol nights (0.4±0.3 spindles/min) compared to Mixer-only (0.9 ± 0.3 spindles/min; F(1,145)=8.33, p&lt;.01)). In the final third of the night, spindle density was conversely higher in the Mixer + Alcohol nights (2.9±1.1 spindles/min) compared to Mixer-only (2.1±0.8 spindles/min; F(1,145)=4.1, p=.03)). No other effects were identified (p’s&gt;.05).

Conclusion
Alcohol use prior to sleep resulted in reduced sleep spindle density early in the night and higher spindle density late in the night. No effects of consecutive nights were observed. These differences add to a growing discussion of the impact that alcohol has on sleep physiology across the night.

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R01AA025593
0049 Sleep and Electroencephalogram Effects from a Dual Orexin Receptor Antagonist in Mice with Traumatic Brain Injury
Authors: Craig John , Carey Sean , Gibbons Allison , Kaplan Gary , Zielinski Mark 
Published: April 2024

Abstract

Introduction
Traumatic brain injuries (TBI) can cause persistent sleep dysregulation regardless of injury severity including hypersomnia, hyposmia, sleepiness, sleep fragmentation, and altered electroencephalogram (EEG) power spectra. Most TBIs are mild in severity, occur in the frontal cortex, and sleep dysregulation can change over time. Orexin targets two receptors that stimulate monoamine release in the brain to promote wakefulness. Our goal was to determine if a dual orexin receptor antagonist (DORA) could improve sleep dysregulation in mice with TBI.

Methods
Two-month-old male and female C57BL/6J mice were randomly assigned to treatment groups. Mice underwent polysomnography surgery. After recovery, mice were administered vehicle by gavage then underwent baseline sleep recordings for 24 h followed by a multiple sleep latency test (MSLT). Mice received a craniectomy and mild/moderate TBI via controlled cortical impact or only a craniectomy serving as a control. A DORA or vehicle were given by gavage, and sleep and MSLT were recorded 24 h, 2 wks, 1 m, and 2 m post-TBI. Sleep state amounts and episode durations and frequencies, sleep latency, and EEG power spectra (0-40 Hz) were determined with significance set at p&lt; 0.05.

Results
In mice given the DORA or vehicle, non-rapid-eye movement (NREM) sleep was significantly increased 24 h after TBI compared to controls. Conversely, NREM sleep was significantly reduced 2 m post-TBI in both vehicle and DORA groups. DORA and/or TBI groups had significantly reduced waking episodes 24 h post-injury but increased waking episodes 2 m post-TBI compared to controls indicating sleep fragmentation. Largely, significantly increased sleep latency time in the MSLT was found throughout all times post-injury in the DORA and TBI groups compared to the controls, which suggests increased sleepiness. Relative to controls, TBI significantly increased EEG delta power (0.5-4 Hz) 24 h post-TBI and significantly reduced EEG delta power 2 m post-TBI, although other frequency bands were not affected.

Conclusion
These data suggest that a DORA induces sleepiness but has minimal effects on impaired sleep amounts, sleep fragmentation, sleepiness, and EEG power spectra 2 m after mild/moderate TBI.

Support (if any)
Merit Review Award (I01BX005379)(MRZ) and SPiRE Award (I21RX003722)(GBK) Department of Veterans Affairs
0052 Recovery Nap After Total Sleep Deprivation Restores Emotional Memory Performance to Typically-Rested Levels
Authors: Cunningham Tony , Denis Dan , Bottary Ryan , Kensinger Elizabeth , Zeng Shengzi , Stickgold Robert 
Published: April 2024

Abstract

Introduction
While a brief period of recovery sleep can ameliorate the negative impacts of total sleep deprivation (TSD) on cognitive functioning, the effects of post-TSD recovery sleep on different forms of emotional functioning remain equivocal. Here, we investigated the effects of TSD and post-TSD recovery sleep on emotional memory processing and compared it to typical functioning in a rested condition.

Methods
During encoding of the emotional memory trade-off (ETO) task, participants viewed scenes with negative or neutral central objects overlaid on neutral backgrounds. During recognition, the central objects and backgrounds were presented separately and participants were asked to identify each of them as ‘Old’ or ‘New’. Forty-six participants in the TSD condition and 22 participants in the Sleep condition completed encoding the morning after the sleep manipulation (~10:00) and a recognition test was conducted on half of the scene components after a short delay (Recog_1, ~10:45). Twenty of the TSD participants were then given a 90-min nap opportunity (TSD_Nap). Participants then completed a second recognition test on the remaining images (Recog_2, ~14:00).

Results
At Recog_1, a group effect revealed significantly worse memory after TSD compared to Sleep (p=.02). Specifically, memory was significantly worse for every scene component except neutral objects, and there were no baseline differences between TSD_nap and TSD_NoNap participants. At Recog_2, memory continued to deteriorate for all scene components in the TSD_NoNap group compared to their Recog_1 performance (all p’s&lt; 0.025). The TSD_nap group, however, had no change in memory for any of the neutral scene components and had improved negative object memory (p=.049) driven by a reduced false alarm rate (p&lt;.001). As such, performance in the TSD_nap group matched the Sleep group at Recog_2 (all p’s&gt;0.1).

Conclusion
These results demonstrate that post-TSD recovery sleep preserves and restores memory functioning such that performance matches typically-rested individuals – while extended TSD leads to continued deterioration – highlighting the importance of sleep in healthy emotional memory functioning. Additionally, the ETO effect (i.e., greater disparity between negative objects and their paired backgrounds compared to neutral objects and their backgrounds) was preserved for both recognition tasks in all groups, demonstrating the strength of this memory phenomenon.

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0054 PTSD Severity Moderates the Association Between N3 Nested Sleep Spindles and Emotional Memory
Authors: Richards Anne , Natraj Nikhilesh , Santistevan Anthony , Yack Leslie , Woodward Steven , Mathalon Daniel , Neylan Thomas 
Published: April 2024

Abstract

Introduction
Sleep disturbance is a core feature of posttraumatic stress disorder (PTSD) and may contribute to aberrant emotional memory processing in the disorder. Sleep spindles during N3 sleep that overlap temporally with slow oscillations (nested N3 SO spindles) are thought to play a role in memory consolidation and may be one mechanism through which adaptive memory processes are disrupted in PTSD.

Methods
N = 44 trauma-exposed participants (Mean Age = 32.4 (SD = 6.0), 47.7% female, 86.4% veteran) with variable PTSD severity (Mean CAPS-5 = 15.5 (SD = 10.8)) based on clinician-administered PTSD Scale (CAPS-5) viewed emotional and neutral International Affective Picture Scale (IAPS) images during electroencephalography (EEG) recording. Neurophysiological reactivity in the 300-1000 msec following stimulus presentation (late positive potential (LPP)) was measured. Participants then took a polysomnography (PSG) measured nap from which nested N3 SO spindle rates were derived. Participants’ recall memory of images was assessed post nap. Linear regression was used to test for an interaction between CAPS score and LPP magnitude (emotional minus neutral) in predicting N3 SO spindle rate and to test for an interaction between CAPS score and N3 SO spindle rate in predicting emotional memory measures (emotional hit rate, false alarm rate, and d', controlling for neutral).

Results
Across subjects, the LPP was greater for emotional compared to neutral images (p &lt; 0.001). Furthermore, the association between LPP magnitude and nested N3 SO spindles was moderated by CAPS severity (p = 0.03), such that participants with low CAPS evidenced a positive association between LPP reactivity and nested N3 SO spindle rate (p = 0.048) whereas high CAPS participants showed no association (p = 0.26). We additionally found that associations between nested N3 SO spindle rate and several measures of emotional memory were moderated by CAPS severity (ps &lt; 0.05): higher nested N3 SO spindle rates were correlated with worse memory for emotional images in high CAPS participants (ps &lt; 0.05), but improved memory in low CAPS participants (ps &lt; 0.05).

Conclusion
Results suggest a breakdown in the function of nested N3 SO spindles for emotional memory consolidation in PTSD.

Support (if any)
VA Career Development Award 5IK2CX000871-05 (PI Richards) .
0055 Leptin Moderates the Relationship Between Sleep Quality and Memory Function: A Population-based Study
Authors: Mosini Amanda , Adami Luana , Vallim Julia , Moyses-Oliveira Mariana , Poyares Dalva , Andersen Monica , Tufik Sergio 
Published: April 2024

Abstract

Introduction
Sleep is crucial for memory, as it promotes its encoding, consolidation, storage, and retrieval. Sleep periods following learning enhance memory consolidation. Leptin, a hormone that regulates appetite and energy balance, also influences memory and neuroplasticity. It plays a neurotrophic role in the hippocampus, enhancing synaptic function and promoting memory processes. Given these associations between sleep, memory, and leptin, this study aimed to evaluate the interplay between sleep quality, memory complaints and leptin levels.

Methods
Using data from the São Paulo Epidemiologic Sleep Study (EPISONO) 2007 edition, we analyzed data from 881 participants who underwent evaluations for subjective sleep quality (Pittsburgh Sleep Quality Index), memory function (Prospective and Retrospective Memory Questionnaire), body mass index and plasmatic leptin levels. Linear regression explored variable relationships, and a mediation/moderation model assessed causal effects on sleep quality, memory, and leptin, with age as a covariate. Analyses were performed on all volunteers and separately by sleep quality, considering sex as a potential influence. The statistical software used was Jamovi version 2.3.24, with a significance level set at 5% (p&lt; 0.05).

Results
After confirming that subjects with poor sleep quality had more memory complaints (p&lt; 0.001) in our cohort, we observed that leptin levels were increased in individuals with more memory complaints (p&lt; 0.001) but there was no association between leptin levels and sleep quality (p=0.177). Mediation analysis reinforced the direct effect of sleep quality on memory function, but leptin had no indirect effect as mediator over the sleep-memory association. Moderation analysis revealed that leptin acted as a moderator in the relationship between sleep quality and memory (p&lt; 0.001), with increased leptin levels enhancing the effect of sleep quality over memory function.

Conclusion
Leptin, a hormone involved in appetite control and energy balance, acts as a moderator of the relationship between sleep quality and memory performance. Individuals with high leptin levels are more susceptible to the negative effects of poor sleep on memory. This finding highlights the complexity of the interaction between sleep, memory, and metabolic factors, such as leptin, and its potential implications for overall health and well-being.

Support (if any)
AFIP, FAPESP, CNPq.
0059 A Transformer Model for Predicting Cognitive Impairment from Sleep
Authors: Song Tzu-An , Malekzadeh Masoud , Saxena Richa , Purcell Shaun M · , Dutta Joyita 
Published: April 2024

Abstract

Introduction
Sleep disruptions have been found to have a strong association not only with normal cognitive decline that occurs with age, but also with dementia caused by neurodegenerative diseases such as Alzheimer's disease (AD). Predictive techniques that can automatically detect cognitive impairment from an individual’s sleep patterns have broad clinical and biological significance. We present an innovative multi-task learning paradigm that leverages deep learning to simultaneously predict cognitive performance measured from two distinct cognitive tests, Cognitive Abilities Screening Instrument (CASI) and Digit Symbol Coding Test (DSCT), using whole-night sleep electroencephalography (EEG) data, sleep stage labels, and covariates in an elderly cohort.

Methods
Our study utilizes data obtained from the Multi-Ethnic Study of Atherosclerosis (MESA) participants randomly assigned to two cohorts: validation (N=470) and training (N=1,110). Our approach uses a multi-task transformer architecture to learn complex patterns of sleep architecture for binary cognitive status prediction. The ground truth binary cognitive status labels (low and high score groups) are generated by using the dataset's median CASI and DSCT values as the thresholds. We use sleep EEG, sleep stage labels, and covariates as inputs and binary CASI and DSCT cognitive score classes as targets to train and validate our model.

Results
Our transformer model achieves an overall accuracy (OA) of 70.21% with an F1-score of 71.43% for CASI and 70.85% with an F1-score of 69.35% for DSCT. In comparison, a neural network trained using 132 handcrafted sleep features as inputs has an OA of 59.57% with an F1-score of 60.08% for CASI and 60.64% with an F1-score of 60.04% for DSCT. The OA and F1-score margins are 10.64% and 11.35% for CASI and 10.21% and 9.31% for DSCT, respectively.

Conclusion
We introduced a deep multi-task learning framework for predicting a person's cognitive status using whole-night sleep EEG data. Our transformer model outperforms the comparison method trained using the handcrafted features in OA and F1-score by a large margin. To our knowledge, this is the first deep learning model for jointly predicting cognitive status based on two different testing instruments from an individual’s sleep EEG data.

Support (if any)
This work was supported in part by the NIH grant 1R21AG068890-01.
0064 Sleep Loss Affects Item and Source Memory Differentially as a Function of Serotonin Transporter (5-HTTLPR) Genotype
Authors: Skeiky Lillian , Lundholm Kirsie , Hovland Sean , Whitney Paul , Hinson John , Van Dongen Hans , Kurinec Courtney 
Published: April 2024

Abstract

Introduction
Remembering relationships between items (information) and the contexts (sources) in which they are framed is crucial for everyday functioning. Total sleep deprivation (TSD) impairs this ability, with evidence suggesting that TSD affects source memory even when items are remembered. Source memory deficits imply problems with associative memory, which relies on hippocampal functioning, known to be altered by TSD. Serotonin is highly expressed in the hippocampus, is influenced by TSD, and may be part of a mechanism by which TSD degrades source memory. We investigated the association between 5-HTTLPR, a functional length polymorphism of the human serotonin transporter gene (SLC6A4), and item and source memory during TSD.

Methods
N=34 healthy adults (ages 27.3±4.9y; 18 female) participated in a 4-day/3-night laboratory TSD study. Participants underwent 38h TSD, preceded and followed by 10h sleep opportunities. At baseline and 24h later during TSD, they completed an item/source memory task. Participants listened to a list of 60 words each presented by a male or female speaker (study phase). They were then tested for recognition of the words (items) out of 60 old and 60 new words presented visually, and were asked to identify the corresponding speakers (sources, male or female).

Results
The genotype distribution was in Hardy-Weinberg equilibrium (P=0.34), with 35.3% long/long, 41.2% long/short, 23.5% short/short. Mixed-effects ANOVA showed a significant adverse effect of TSD for both item recognition (P&lt; 0.001) and source recognition (P&lt; 0.001), where TSD degraded source memory even when item recognition was accurate. There were no 5-HTTLPR genotype effects on item memory. However, there was a significant main effect for genotype on source memory (P=0.019), and a genotype by TSD interaction (P=0.018). For accurately recognized items, source memory was largely preserved for the short/short genotype but impaired for carriers of the long allele, and especially the long/long genotype.

Conclusion
5-HTTLPR genotype predicted source memory deficits from TSD, distinct from item memory deficits unaffected by genotype, which confirms that item and source memory deficits due to TSD are dissociable. Furthermore, TSD’s impact on binding of items and sources in memory may be mediated by hippocampal serotonin.

Support (if any)
NIH R21CA167691, WSU Anthony Marchionne and Foundry10 Bridge fellowships