Effect of 1 Night of Total Sleep Deprivation on Cerebrospinal Fluid β-Amyloid 42 in Healthy Middle-Aged Men

The sleep-wake cycle regulates interstitial fluid (ISF) and cerebrospinal fluid (CSF) levels of β-amyloid (Aβ) that accumulates in Alzheimer’s disease (AD). Furthermore, chronic sleep deprivation (SD) increases Aβ plaques. However, tau, not Aβ, accumulation appears to drive AD neurodegeneration. We tested whether ISF/CSF tau and tau seeding and spreading were influenced by the sleep-wake cycle and SD. Mouse ISF tau was increased ~90% during normal wakefulness versus sleep and ~100% during SD. Human CSF tau also increased more than 50% during SD. In a tau seeding-and-spreading model, chronic SD increased tau pathology spreading. Chemogenetically driven wakefulness in mice also significantly increased both ISF Aβ and tau. Thus, the sleep-wake cycle regulates ISF tau, and SD increases ISF and CSF tau as well as tau pathology spreading.

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Supplemental Material for Short-Term Total Sleep Deprivation Alters Delay-Conditioned Memory in the Rat

Behavioral Neuroscience ◽

10.1037/bne0000136.supp ◽

2016 ◽

Keyword(s):

Sleep Deprivation ◽

Short Term ◽

Total Sleep Deprivation

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Altered Functional Connectivity between the Nucleus Basalis of Meynert and Anterior Cingulate Cortex is Associated with Declined Attentional Performance after Total Sleep Deprivation

Behavioural Brain Research ◽

10.1016/j.bbr.2021.113321 ◽

2021 ◽

pp. 113321

Author(s):

Jing Qi ◽

Bo-Zhi Li ◽

Ying Zhang ◽

Bei Pan ◽

Yu-Hong Gao ◽

...

Keyword(s):

Functional Connectivity ◽

Sleep Deprivation ◽

Anterior Cingulate Cortex ◽

Cingulate Cortex ◽

Anterior Cingulate ◽

Nucleus Basalis ◽

Nucleus Basalis Of Meynert ◽

Total Sleep Deprivation ◽

Attentional Performance

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Residual, differential neurobehavioral deficits linger after multiple recovery nights following chronic sleep restriction or acute total sleep deprivation

SLEEP ◽

10.1093/sleep/zsaa224 ◽

2020 ◽

Author(s):

Erika M Yamazaki ◽

Caroline A Antler ◽

Charlotte R Lasek ◽

Namni Goel

Keyword(s):

Sleep Deprivation ◽

Response Speed ◽

Sleep Loss ◽

Sleep Restriction ◽

Total Sleep Deprivation ◽

Psychomotor Vigilance Test ◽

Recovery Sleep ◽

Time In Bed ◽

Neurobehavioral Deficits ◽

Chronic Sleep

Abstract Study Objectives The amount of recovery sleep needed to fully restore well-established neurobehavioral deficits from sleep loss remains unknown, as does whether the recovery pattern differs across measures after total sleep deprivation (TSD) and chronic sleep restriction (SR). Methods In total, 83 adults received two baseline nights (10–12-hour time in bed [TIB]) followed by five 4-hour TIB SR nights or 36-hour TSD and four recovery nights (R1–R4; 12-hour TIB). Neurobehavioral tests were completed every 2 hours during wakefulness and a Maintenance of Wakefulness Test measured physiological sleepiness. Polysomnography was collected on B2, R1, and R4 nights. Results TSD and SR produced significant deficits in cognitive performance, increases in self-reported sleepiness and fatigue, decreases in vigor, and increases in physiological sleepiness. Neurobehavioral recovery from SR occurred after R1 and was maintained for all measures except Psychomotor Vigilance Test (PVT) lapses and response speed, which failed to completely recover. Neurobehavioral recovery from TSD occurred after R1 and was maintained for all cognitive and self-reported measures, except for vigor. After TSD and SR, R1 recovery sleep was longer and of higher efficiency and better quality than R4 recovery sleep. Conclusions PVT impairments from SR failed to reverse completely; by contrast, vigor did not recover after TSD; all other deficits were reversed after sleep loss. These results suggest that TSD and SR induce sustained, differential biological, physiological, and/or neural changes, which remarkably are not reversed with chronic, long-duration recovery sleep. Our findings have critical implications for the population at large and for military and health professionals.

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Muscle temperature is least altered during total sleep deprivation in rats

Journal of Thermal Biology ◽

10.1016/j.jtherbio.2021.102910 ◽

2021 ◽

pp. 102910

Author(s):

Binney Sharma ◽

Trina Sengupta ◽

Lal Chandra Vishwakarma ◽

Nasreen Akhtar ◽

Hruda Nanda Mallick

Keyword(s):

Sleep Deprivation ◽

Muscle Temperature ◽

Total Sleep Deprivation

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0308 DRD2 C957T Genotype Influences Vigilant Attention Performance Impairment During Total Sleep Deprivation

SLEEP ◽

10.1093/sleep/zsaa056.305 ◽

2020 ◽

Vol 43 (Supplement_1) ◽

pp. A116-A116

Author(s):

R A Muck ◽

L Skeiky ◽

M A Schmidt ◽

B C Satterfield ◽

J P Wisor ◽

...

Keyword(s):

Sleep Deprivation ◽

Analysis Of Covariance ◽

Genotype Distribution ◽

Total Sleep Deprivation ◽

Psychomotor Vigilance Test ◽

Time In Bed ◽

Dat1 Gene ◽

Performance Impairment ◽

Attention Performance ◽

Time Awake

Abstract Introduction There are substantial, phenotypical individual differences in the adverse impact of total sleep deprivation (TSD) on vigilant attention performance. Dopaminergic genotypes have been found to contribute to these phenotypical differences. Here we investigated the association between a single nucleotide polymorphism (SNP) of the dopamine receptor D2 (DRD2) gene, C957T (rs6277), on vigilant attention performance measured with the psychomotor vigilance test (PVT) in a laboratory TSD study. Methods N=46 healthy adults (ages 26.0±5.3y; 25 females) completed a 4-day in-laboratory study with a baseline day (10h time in bed: 22:00-08:00), a 38h TSD period, and a recovery day (10h time in bed: 22:00-08:00). DNA isolated from whole blood was assayed for DRD2 C957T genotype using real-time polymerase chain reaction. PVT performance was measured during TSD at 2-4h intervals, and analyzed for genotype using mixed-effects analysis of covariance of lapses of attention (RTs>500ms). Results The genotype distribution in this sample - 28.3% C/C, 50.0% C/T, 21.7% T/T - was found to be in Hardy-Weinberg Equilibrium (X21=0.0008, p=0.98). As expected, there was a significant effect of time awake on PVT performance (F14,602=26.67, p<0.001). There was a significant main effect of DRD2 genotype (F2,602=3.24, p=0.040) and a significant interaction of time awake by DRD2 genotype (F28,602=1.96, p=0.003). Subjects homozygous for the T allele showed greater impairment during extended wakefulness than carriers of the C allele. Genotype explained 7.6% of the variance in the PVT data observed during the 38h TSD period. Conclusion Subjects homozygous for the T allele of DRD2 C957T were considerably more vulnerable to TSD-induced PVT performance impairment than carriers of the C allele. A recent study showed that DRD2 C957T influences PVT performance in interaction with a SNP of the DAT1 gene. Here, DRD2 genotype was by itself also associated with PVT performance impairment during TSD. Support CDMRP awards W81XWH-16-1-0319 and W81XWH-18-1-0100.

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Partial and Total Sleep Deprivation Interferes With Neural Correlates of Consolidation of Fear Extinction Memory

Biological Psychiatry ◽

10.1016/j.biopsych.2021.02.449 ◽

2021 ◽

Vol 89 (9) ◽

pp. S176

Author(s):

Jeehye Seo ◽

Edward F. Pace-Schott ◽

Mohammed R. Milad ◽

Huijin Song ◽

Anne Germain

Keyword(s):

Sleep Deprivation ◽

Neural Correlates ◽

Fear Extinction ◽

Total Sleep Deprivation ◽

Extinction Memory

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Effect of Patient-Specific Preanalytic Variables on CSF Aβ1–42 Concentrations Measured on an Automated Chemiluminescent Platform

The Journal of Applied Laboratory Medicine ◽

10.1093/jalm/jfaa145 ◽

2020 ◽

Author(s):

Jacqueline A Darrow ◽

Amanda Calabro ◽

Sara Gannon ◽

Amanze Orusakwe ◽

Rianne Esquivel ◽

...

Keyword(s):

Cerebrospinal Fluid ◽

Cognitive Impairment ◽

Patient Specific ◽

Csf Biomarkers ◽

Clinical Settings ◽

Blood Contamination ◽

Gradient Effect ◽

Β Amyloid ◽

The Impact ◽

Gradient Effects

Abstract Background Cerebrospinal fluid (CSF) biomarkers are increasingly used to confirm the accuracy of a clinical diagnosis of mild cognitive impairment or dementia due to Alzheimer disease (AD). Recent evidence suggests that fully automated assays reduce the impact of some preanalytical factors on the variability of these measures. This study evaluated the effect of several preanalytical variables common in clinical settings on the variability of CSF β-amyloid 1–42 (Aβ1–42) concentrations. Methods Aβ1–42 concentrations were measured using the LUMIPULSE G1200 from both freshly collected and frozen CSF samples. Preanalytic variables examined were: (1) patient fasting prior to CSF collection, (2) blood contamination of specimens, and (3) aliquoting specimens sequentially over the course of collection (i.e., CSF gradients). Results Patient fasting did not significantly affect CSF Aβ1–42 levels. While assessing gradient effects, Aβ1–42 concentrations remained stable within the first 5 1-mL aliquots. However, there is evidence of a gradient effect toward higher concentrations over successive aliquots. Aβ1–42 levels were stable when fresh CSF samples were spiked with up to 2.5% of blood. However, in frozen CSF samples, even 0.25% blood contamination significantly decreased Aβ1–42 concentrations. Conclusions The preanalytical variables examined here do not have significant effects on Aβ1–42 concentrations if fresh samples are processed within 2 h. However, a gradient effect can be observed on Aβ1–42 concentrations after the first 5 mL of collection and blood contamination has a significant impact on Aβ1–42 concentrations once specimens have been frozen.

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137 Recovery Dynamics in a Biomathematical Model of Fatigue

SLEEP ◽

10.1093/sleep/zsab072.136 ◽

2021 ◽

Vol 44 (Supplement_2) ◽

pp. A56-A56

Author(s):

Mark McCauley ◽

Peter McCauley ◽

Hans Van Dongen

Keyword(s):

Sleep Deprivation ◽

Goodness Of Fit ◽

Sleep Loss ◽

Sleep Restriction ◽

Commercial Aviation ◽

Circadian Misalignment ◽

Total Sleep Deprivation ◽

Homeostatic Process ◽

Recovery Sleep

Abstract Introduction In commercial aviation and other operational settings where biomathematical models of fatigue are used for fatigue risk management, accurate prediction of recovery during rest periods following duty periods with sleep loss and/or circadian misalignment is critical. The recuperative potential of recovery sleep is influenced by a variety of factors, including long-term, allostatic effects of prior sleep/wake history. For example, recovery tends to be slower after sustained sleep restriction versus acute total sleep deprivation. Capturing such dynamics has proven to be challenging. Methods Here we focus on the dynamic biomathematical model of McCauley et al. (2013). In addition to a circadian process, this model features differential equations for sleep/wake regulation including a short-term sleep homeostatic process capturing change in the order of hours/days and a long-term allostatic process capturing change in the order of days/weeks. The allostatic process modulates the dynamics of the homeostatic process by shifting its equilibrium setpoint, which addresses recently observed phenomena such as reduced vulnerability to sleep loss after banking sleep. It also differentiates the build-up and recovery rates of fatigue under conditions of chronic sleep restriction versus acute total sleep deprivation; nonetheless, it does not accurately predict the disproportionately rapid recovery seen after total sleep deprivation. To improve the model, we hypothesized that the homeostatic process may also modulate the allostatic process, with the magnitude of this effect scaling as a function of time awake. Results To test our hypothesis, we added a parameter to the model to capture modulation by the homeostatic process of the allostatic process build-up during wakefulness and dissipation during sleep. Parameter estimation using previously published laboratory datasets of fatigue showed this parameter as significantly different from zero (p<0.05) and yielding a 10%–20% improvement in goodness-of-fit for recovery without adversely affecting goodness-of-fit for pre-recovery days. Conclusion Inclusion of a modulation effect of the allostatic process by the homeostatic process improved prediction accuracy in a variety of sleep loss and circadian misalignment scenarios. In addition to operational relevance for duty/rest scheduling, this finding has implications for understanding mechanisms underlying the homeostatic and allostatic processes of sleep/wake regulation. Support (if any) Federal Express Corporation

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