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Article ; Online: NREM delta power and AD-relevant tauopathy are associated with shared cortical gene networks.

Scarpa, Joseph R / Jiang, Peng / Gao, Vance D / Vitaterna, Martha H / Turek, Fred W / Kasarskis, Andrew

2021 Volume 11, Issue 1, Page(s) 7797

Abstract: Reduced NREM sleep in humans is associated with AD neuropathology. Recent work has demonstrated a reduction in NREM sleep in preclinical AD, pointing to its potential utility as an early marker of dementia. We test the hypothesis that reduced NREM delta ... ...

Abstract	Reduced NREM sleep in humans is associated with AD neuropathology. Recent work has demonstrated a reduction in NREM sleep in preclinical AD, pointing to its potential utility as an early marker of dementia. We test the hypothesis that reduced NREM delta power and increased tauopathy are associated with shared underlying cortical molecular networks in preclinical AD. We integrate multi-omics data from two extensive public resources, a human Alzheimer's disease cohort from the Mount Sinai Brain Bank (N = 125) reflecting AD progression and a (C57BL/6J × 129S1/SvImJ) F2 mouse population in which NREM delta power was measured (N = 98). Two cortical gene networks, including a CLOCK-dependent circadian network, are associated with NREM delta power and AD tauopathy progression. These networks were validated in independent mouse and human cohorts. Identifying gene networks related to preclinical AD elucidate possible mechanisms associated with the early disease phase and potential targets to alter the disease course.
MeSH term(s)	Alzheimer Disease/pathology ; Animals ; Cerebellar Cortex/metabolism ; Cohort Studies ; Gene Regulatory Networks ; Humans ; Mice ; Mice, Inbred C57BL ; Sleep Wake Disorders/pathology
Language	English
Publishing date	2021-04-08
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-021-86255-6
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Article ; Online: Casein kinase 1 epsilon and circadian misalignment impact affective behaviours in mice.

Zhou, Lili / Fitzpatrick, Karrie / Olker, Christopher / Vitaterna, Martha H / Turek, Fred W

The European journal of neuroscience

2021 Volume 55, Issue 9-10, Page(s) 2939–2954

Abstract: Affective behaviours and mental health are profoundly affected by disturbances in circadian rhythms. Casein kinase 1 epsilon (CSNK1E) is a core component of the circadian clock. Mice with tau or null mutation of this gene have shortened and lengthened ... ...

Abstract	Affective behaviours and mental health are profoundly affected by disturbances in circadian rhythms. Casein kinase 1 epsilon (CSNK1E) is a core component of the circadian clock. Mice with tau or null mutation of this gene have shortened and lengthened circadian period respectively. Here, we examined anxiety-like, fear, and despair behaviours in both male and female mice of these two different mutants. Compared with wild-type mice, we found reductions in fear and anxiety-like behaviours in both mutant lines and in both sexes, with the tau mutants exhibiting the greatest phenotypic changes. However, the behavioural despair had distinct phenotypic patterns, with markedly less behavioural despair in female null mutants, but not in tau mutants of either sex. To determine whether abnormal light entrainment of tau mutants to 24-h light-dark cycles contributes to these phenotypic differences, we also examined these behaviours in tau mutants on a 20-h light-dark cycle close to their endogenous circadian period. The normalized entrainment restored more wild-type-like behaviours for fear and anxiety, but it induced behavioural despair in tau mutant females. These data show that both mutations of Csnk1e broadly affect fear and anxiety-like behaviours, while the effects on behavioural despair vary with genetics, photoperiod, and sex, suggesting that the mechanisms by which Csnk1e affects fear and anxiety-like behaviours may be similar, but distinct from those affecting behavioural despair. Our study also provides experimental evidence in support of the hypothesis of beneficial outcomes from properly entrained circadian rhythms in terms of the anxiety-like and fear behaviours.
MeSH term(s)	Animals ; Casein Kinase 1 epsilon/genetics ; Circadian Clocks ; Circadian Rhythm/genetics ; Female ; Male ; Mice ; Motor Activity ; Photoperiod
Chemical Substances	Casein Kinase 1 epsilon (EC 2.7.11.1)
Language	English
Publishing date	2021-09-23
Publishing country	France
Document type	Journal Article
ZDB-ID	645180-9
ISSN	1460-9568 ; 0953-816X
ISSN (online)	1460-9568
ISSN	0953-816X
DOI	10.1111/ejn.15456
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Article ; Online: Dopamine pathway imbalance in mice lacking Magel2, a Prader-Willi syndrome candidate gene.

Luck, Chloe / Vitaterna, Martha H / Wevrick, Rachel

Behavioral neuroscience

2016 Volume 130, Issue 4, Page(s) 448–459

Abstract: The etiology of abnormal eating behaviors, including binge-eating disorder, is poorly understood. The neural circuits modulating the activities of the neurotransmitters dopamine and serotonin are proposed to be dysfunctional in individuals suffering from ...

Abstract	The etiology of abnormal eating behaviors, including binge-eating disorder, is poorly understood. The neural circuits modulating the activities of the neurotransmitters dopamine and serotonin are proposed to be dysfunctional in individuals suffering from eating disorders. Prader-Willi syndrome is a neurodevelopmental disorder that causes extreme food seeking and binge-eating behaviors together with reduced satiety. One of the genes implicated in Prader-Willi syndrome, Magel2, is highly expressed in the regions of the brain that control appetite. Our objective was to examine behaviors relevant to feeding and the neural circuits controlling feeding in a mouse model of Prader-Willi syndrome that lacks expression of the Magel2 gene. We performed behavioral tests related to dopaminergic function, measuring cocaine-induced hyperlocomotion, binge eating, and saccharin-induced anhedonia in Magel2-deficient mice. Next, we analyzed dopaminergic neurons in various brain regions and compared these findings between genotypes. Finally, we examined biochemical markers in the brain under standard diet, high-fat diet, and withdrawal from a high-fat diet conditions. We identified abnormal behaviors and biomarkers reflecting dopaminergic dysfunction in mice lacking Magel2. Our results provide a biological framework for clinical studies of dopaminergic function in children with Prader-Willi syndrome, and may also provide insight into binge-eating disorders that occur in the general population. (PsycINFO Database Record
Language	English
Publishing date	2016
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	230159-3
ISSN	1939-0084 ; 0735-7044
ISSN (online)	1939-0084
ISSN	0735-7044
DOI	10.1037/bne0000150
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Zs.A 1837: Show issues

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Article: A Prebiotic Diet Alters the Fecal Microbiome and Improves Sleep in Response to Sleep Disruption in Rats.

Bowers, Samuel J / Summa, Keith C / Thompson, Robert S / González, Antonio / Vargas, Fernando / Olker, Christopher / Jiang, Peng / Lowry, Christopher A / Dorrestein, Pieter C / Knight, Rob / Wright, Kenneth P / Fleshner, Monika / Turek, Fred W / Vitaterna, Martha H

Frontiers in neuroscience

2022 Volume 16, Page(s) 889211

Abstract: Sleep disruption is a challenging and exceedingly common physiological state that contributes to a wide range of biochemical and molecular perturbations and has been linked to numerous adverse health outcomes. Modern society exerts significant pressure ... ...

Abstract	Sleep disruption is a challenging and exceedingly common physiological state that contributes to a wide range of biochemical and molecular perturbations and has been linked to numerous adverse health outcomes. Modern society exerts significant pressure on the sleep/wake cycle
Language	English
Publishing date	2022-05-24
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2411902-7
ISSN	1662-453X ; 1662-4548
ISSN (online)	1662-453X
ISSN	1662-4548
DOI	10.3389/fnins.2022.889211
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Article ; Online: Immunization with a heat-killed bacterium, Mycobacterium vaccae NCTC 11659, prevents the development of cortical hyperarousal and a PTSD-like sleep phenotype after sleep disruption and acute stress in mice.

Bowers, Samuel J / Lambert, Sophie / He, Shannon / Lowry, Christopher A / Fleshner, Monika / Wright, Kenneth P / Turek, Fred W / Vitaterna, Martha H

Sleep

2020 Volume 44, Issue 6

Abstract: Study objectives: Sleep deprivation induces systemic inflammation that may contribute to stress vulnerability and other pathologies. We tested the hypothesis that immunization with heat-killed Mycobacterium vaccae NCTC 11659 (MV), an environmental ... ...

Abstract	Study objectives: Sleep deprivation induces systemic inflammation that may contribute to stress vulnerability and other pathologies. We tested the hypothesis that immunization with heat-killed Mycobacterium vaccae NCTC 11659 (MV), an environmental bacterium with immunoregulatory and anti-inflammatory properties, prevents the negative impacts of 5 days of sleep disruption on stress-induced changes in sleep, behavior, and physiology in mice. Methods: In a 2 × 2 × 2 experimental design, male C57BL/6N mice were given injections of either MV or vehicle on days -17, -10, and -3. On days 1-5, mice were exposed to intermittent sleep disruption, whereby sleep was disrupted for 20 h per day. Immediately following sleep disruption, mice were exposed to 1-h social defeat stress or novel cage (control) conditions. Object location memory (OLM) testing was conducted 24 h after social defeat, and tissues were collected 6 days later to measure inflammatory markers. Sleep was recorded using electroencephalography (EEG) and electromyography (EMG) throughout the experiment. Results: In vehicle-treated mice, only the combination of sleep disruption followed by social defeat (double hit): (1) increased brief arousals and NREM beta (15-30 Hz) EEG power in sleep immediately post-social defeat compared to baseline; (2) induced an increase in the proportion of rapid-eye-movement (REM) sleep and number of state shifts for at least 5 days post-social defeat; and (3) induced hyperlocomotion and lack of habituation in the OLM task. Immunization with MV prevented most of these sleep and behavioral changes. Conclusions: Immunization with MV ameliorates a stress-induced sleep and behavioral phenotype that shares features with human posttraumatic stress disorder.
MeSH term(s)	Animals ; Arousal ; Electroencephalography ; Hot Temperature ; Immunization ; Male ; Mice ; Mice, Inbred C57BL ; Mycobacteriaceae ; Mycobacterium ; Phenotype ; Sleep ; Stress Disorders, Post-Traumatic
Language	English
Publishing date	2020-12-07
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	424441-2
ISSN	1550-9109 ; 0161-8105
ISSN (online)	1550-9109
ISSN	0161-8105
DOI	10.1093/sleep/zsaa271
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Zs.A 1475: Show issues

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Article: Altered Body Weight Regulation in CK1ε Null and tau Mutant Mice on Regular Chow and High Fat Diets.

Zhou, Lili / Summa, Keith C / Olker, Christopher / Vitaterna, Martha H / Turek, Fred W

Genetics research international

2016 Volume 2016, Page(s) 4973242

Abstract: Disruption of circadian rhythms results in metabolic dysfunction. Casein kinase 1 epsilon (CK1ε) is a canonical circadian clock gene. Null and tau mutations in CK1ε show distinct effects on circadian period. To investigate the role of CK1ε in body weight ...

Abstract	Disruption of circadian rhythms results in metabolic dysfunction. Casein kinase 1 epsilon (CK1ε) is a canonical circadian clock gene. Null and tau mutations in CK1ε show distinct effects on circadian period. To investigate the role of CK1ε in body weight regulation under both regular chow (RC) and high fat (HF) diet conditions, we examined body weight on both RC and HF diets in CK1ε (-/-) and CK1ε (tau/tau) mice on a standard 24 hr light-dark (LD) cycle. Given the abnormal entrainment of CK1ε (tau/tau) mice on a 24 hr LD cycle, a separate set of CK1ε (tau/tau) mice were tested under both diet conditions on a 20 hr LD cycle, which more closely matches their endogenous period length. On the RC diet, both CK1ε (-/-) and CK1ε (tau/tau) mutants on a 24 hr LD cycle and CK1ε (tau/tau) mice on a 20 hr LD cycle exhibited significantly lower body weights, despite similar overall food intake and activity levels. On the HF diet, CK1ε (tau/tau) mice on a 20 hr LD cycle were protected against the development of HF diet-induced excess weight gain. These results provide additional evidence supporting a link between circadian rhythms and energy regulation at the genetic level, particularly highlighting CK1ε involved in the integration of circadian biology and metabolic physiology.
Language	English
Publishing date	2016-04-06
Publishing country	Egypt
Document type	Journal Article
ZDB-ID	2662558-1
ISSN	2090-3162 ; 2090-3154
ISSN (online)	2090-3162
ISSN	2090-3154
DOI	10.1155/2016/4973242
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Article ; Online: Repeated sleep disruption in mice leads to persistent shifts in the fecal microbiome and metabolome.

Bowers, Samuel J / Vargas, Fernando / González, Antonio / He, Shannon / Jiang, Peng / Dorrestein, Pieter C / Knight, Rob / Wright, Kenneth P / Lowry, Christopher A / Fleshner, Monika / Vitaterna, Martha H / Turek, Fred W

PloS one

2020 Volume 15, Issue 2, Page(s) e0229001

Abstract: It has been established in recent years that the gut microbiome plays a role in health and disease, potentially via alterations in metabolites that influence host physiology. Although sleep disruption and gut dysbiosis have been associated with many of ... ...

Abstract	It has been established in recent years that the gut microbiome plays a role in health and disease, potentially via alterations in metabolites that influence host physiology. Although sleep disruption and gut dysbiosis have been associated with many of the same diseases, studies investigating the gut microbiome in the context of sleep disruption have yielded inconsistent results, and have not assessed the fecal metabolome. We exposed mice to five days of sleep disruption followed by four days of ad libitum recovery sleep, and assessed the fecal microbiome and fecal metabolome at multiple timepoints using 16S rRNA gene amplicons and untargeted LC-MS/MS mass spectrometry. We found global shifts in both the microbiome and metabolome in the sleep-disrupted group on the second day of recovery sleep, when most sleep parameters had recovered to baseline levels. We observed an increase in the Firmicutes:Bacteroidetes ratio, along with decreases in the genus Lactobacillus, phylum Actinobacteria, and genus Bifidobacterium in sleep-disrupted mice compared to control mice. The latter two taxa remained low at the fourth day post-sleep disruption. We also identified multiple classes of fecal metabolites that were differentially abundant in sleep-disrupted mice, some of which are physiologically relevant and commonly influenced by the microbiome. This included bile acids, and inference of microbial functional gene content suggested reduced levels of the microbial bile salt hydrolase gene in sleep-disrupted mice. Overall, this study adds to the evidence base linking disrupted sleep to the gut microbiome and expands it to the fecal metabolome, identifying sleep disruption-sensitive bacterial taxa and classes of metabolites that may serve as therapeutic targets to improve health after poor sleep.
MeSH term(s)	Animals ; Bacteria/classification ; Bacteria/genetics ; Bacteria/growth & development ; Feces/microbiology ; Gastrointestinal Microbiome ; Male ; Mice ; RNA, Bacterial/genetics ; RNA, Ribosomal, 16S/genetics ; Sleep Deprivation/microbiology
Chemical Substances	RNA, Bacterial ; RNA, Ribosomal, 16S
Language	English
Publishing date	2020-02-20
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0229001
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Article ; Online: Trait-like vulnerability of higher-order cognition and ability to maintain wakefulness during combined sleep restriction and circadian misalignment.

Sprecher, Kate E / Ritchie, Hannah K / Burke, Tina M / Depner, Christopher M / Smits, Alexandra N / Dorrestein, Pieter C / Fleshner, Monika / Knight, Rob / Lowry, Christopher A / Turek, Fred W / Vitaterna, Martha H / Wright, Kenneth P

Sleep

2019 Volume 42, Issue 8

Abstract: Study objectives: Determine stability of individual differences in executive function, cognitive processing speed, selective visual attention, and maintenance of wakefulness during simulated sustained operations with combined sleep restriction and ... ...

Abstract	Study objectives: Determine stability of individual differences in executive function, cognitive processing speed, selective visual attention, and maintenance of wakefulness during simulated sustained operations with combined sleep restriction and circadian misalignment. Methods: Twenty healthy adults (eight female), aged 25.7 (±4.2 SD), body mass index (BMI) 22.3 (±2.1) kg/m2 completed an 18-day protocol twice. Participants maintained habitual self-selected 8-hour sleep schedules for 2 weeks at home prior to a 4-day laboratory visit that included one sleep opportunity per day: 8 hours on night 1, 3 hours on night 2, and 3 hours on mornings 3 and 4. After 3 days of unscheduled sleep at home, participants repeated the entire protocol. Stability and task dependency of individual differences in performance were quantified by intra-class correlation coefficients (ICC) and Kendall's Tau, respectively. Results: Performance on Stroop, Visual Search, and the Maintenance of Wakefulness Test were highly consistent within individuals during combined sleep restriction and circadian misalignment. Individual differences were trait-like as indicated by ICCs (0.54-0.96) classified according to standard criteria as moderate to almost perfect. Individual differences on other performance tasks commonly reported in sleep studies showed fair to almost perfect ICCs (0.22-0.94). Kendall's rank correlations showed that individual vulnerability to sleep restriction and circadian misalignment varied by task and by metric within a task. Conclusions: Consistent vulnerability of higher-order cognition and maintenance of wakefulness to combined sleep restriction and circadian misalignment has implications for the development of precision countermeasure strategies for workers performing safety-critical tasks, e.g. military, police, health care workers and emergency responders.
MeSH term(s)	Adult ; Attention/physiology ; Circadian Rhythm/physiology ; Cognition/physiology ; Executive Function/physiology ; Female ; Humans ; Individuality ; Male ; Polysomnography ; Psychomotor Performance/physiology ; Sleep/physiology ; Sleep Deprivation/physiopathology ; Sleep Disorders, Circadian Rhythm/physiopathology ; Task Performance and Analysis ; Wakefulness/physiology
Language	English
Publishing date	2019-05-07
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	424441-2
ISSN	1550-9109 ; 0161-8105
ISSN (online)	1550-9109
ISSN	0161-8105
DOI	10.1093/sleep/zsz113
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Zs.A 1475: Show issues

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ab Jg. 2022: Lesesaal (EG)

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Article ; Online: NMDAR activation regulates the daily rhythms of sleep and mood.

Burgdorf, Jeffrey S / Vitaterna, Martha H / Olker, Christopher J / Song, Eun Joo / Christian, Edward P / Sørensen, Laurits / Turek, Fred W / Madsen, Torsten M / Khan, M Amin / Kroes, Roger A / Moskal, Joseph R

Sleep

2019 Volume 42, Issue 10

Abstract: Study objectives: The present studies examine the effects of NMDAR activation by NYX-2925 diurnal rhythmicity of both sleep and wake as well as emotion.: Methods: Twenty-four-hour sleep EEG recordings were obtained in sleep-deprived and non-sleep- ... ...

Abstract	Study objectives: The present studies examine the effects of NMDAR activation by NYX-2925 diurnal rhythmicity of both sleep and wake as well as emotion. Methods: Twenty-four-hour sleep EEG recordings were obtained in sleep-deprived and non-sleep-deprived rats. In addition, the day-night cycle of both activity and mood was measured using home cage ultrasonic-vocalization recordings. Results: NYX-2925 significantly facilitated non-REM (NREM) sleep during the lights-on (sleep) period, and this effect persisted for 3 days following a single dose in sleep-deprived rats. Sleep-bout duration and REM latencies were increased without affecting total REM sleep, suggesting better sleep quality. In addition, delta power during wake was decreased, suggesting less drowsiness. NYX-2925 also rescued learning and memory deficits induced by sleep deprivation, measured using an NMDAR-dependent learning task. Additionally, NYX-2925 increased positive affect and decreased negative affect, primarily by facilitating the transitions from sleep to rough-and-tumble play and back to sleep. In contrast to NYX-2925, the NMDAR antagonist ketamine acutely (1-4 hours post-dosing) suppressed REM and non-REM sleep, increased delta power during wake, and blunted the amplitude of the sleep-wake activity rhythm. Discussion: These data suggest that NYX-2925 could enhance behavioral plasticity via improved sleep quality as well as vigilance during wake. As such, the facilitation of sleep by NYX-2925 has the potential to both reduce symptom burden on neurological and psychiatric disorders as well as serve as a biomarker for drug effects through restoration of sleep architecture.
MeSH term(s)	Affect/drug effects ; Affect/physiology ; Animals ; Circadian Rhythm/drug effects ; Circadian Rhythm/physiology ; Electroencephalography/methods ; Male ; Rats ; Rats, Sprague-Dawley ; Receptors, N-Methyl-D-Aspartate/agonists ; Receptors, N-Methyl-D-Aspartate/physiology ; Sleep/drug effects ; Sleep/physiology ; Sleep Deprivation/drug therapy ; Sleep Deprivation/physiopathology ; Spiro Compounds/pharmacology ; Spiro Compounds/therapeutic use ; Wakefulness/drug effects ; Wakefulness/physiology
Chemical Substances	NYX-2925 ; Receptors, N-Methyl-D-Aspartate ; Spiro Compounds
Language	English
Publishing date	2019-09-10
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	424441-2
ISSN	1550-9109 ; 0161-8105
ISSN (online)	1550-9109
ISSN	0161-8105
DOI	10.1093/sleep/zsz135
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Article ; Online: Cross-species systems analysis identifies gene networks differentially altered by sleep loss and depression.

Scarpa, Joseph R / Jiang, Peng / Gao, Vance D / Fitzpatrick, Karrie / Millstein, Joshua / Olker, Christopher / Gotter, Anthony / Winrow, Christopher J / Renger, John J / Kasarskis, Andrew / Turek, Fred W / Vitaterna, Martha H

Science advances

2018 Volume 4, Issue 7, Page(s) eaat1294

Abstract: To understand the transcriptomic organization underlying sleep and affective function, we studied a population of (C57BL/6J × 129S1/SvImJ) F2 mice by measuring 283 affective and sleep phenotypes and profiling gene expression across four brain regions. We ...

Abstract	To understand the transcriptomic organization underlying sleep and affective function, we studied a population of (C57BL/6J × 129S1/SvImJ) F2 mice by measuring 283 affective and sleep phenotypes and profiling gene expression across four brain regions. We identified converging molecular bases for sleep and affective phenotypes at both the single-gene and gene-network levels. Using publicly available transcriptomic datasets collected from sleep-deprived mice and patients with major depressive disorder (MDD), we identified three cortical gene networks altered by the sleep/wake state and depression. The network-level actions of sleep loss and depression were opposite to each other, providing a mechanistic basis for the sleep disruptions commonly observed in depression, as well as the reported acute antidepressant effects of sleep deprivation. We highlight one particular network composed of circadian rhythm regulators and neuronal activity-dependent immediate-early genes. The key upstream driver of this network,
MeSH term(s)	Animals ; Antidepressive Agents/therapeutic use ; Brain/metabolism ; Cerebral Cortex/metabolism ; Circadian Rhythm/genetics ; Depressive Disorder, Major/drug therapy ; Depressive Disorder, Major/genetics ; Depressive Disorder, Major/pathology ; Disease Models, Animal ; Gene Regulatory Networks ; Genotype ; Male ; Mice ; Mice, Inbred C57BL ; Phenotype ; Quantitative Trait Loci ; Sleep Deprivation/drug therapy ; Sleep Deprivation/genetics ; Sleep Deprivation/pathology ; Transcriptome
Chemical Substances	Antidepressive Agents
Language	English
Publishing date	2018-07-25
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2810933-8
ISSN	2375-2548 ; 2375-2548
ISSN (online)	2375-2548
ISSN	2375-2548
DOI	10.1126/sciadv.aat1294
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