Sleep Deprivation Induced Plasma Amyloid-β Transport Disturbance in Healthy Young Adults

Wang, Meng; Zhao, Beiyu; Huo, Kang; Deng, Yongning; Shang, Suhang; Liu, Jie; Li, Yanbo; Ma, Louyan; Jiang, Yu; Dang, Liangjun; Chen, Chen; Shan, Wei; Zhang, Juanli; Yang, Hailei; Gao, Fan; Qu, Qing

doi:10.3233/jad-161213

Cited by 50 publications

(33 citation statements)

References 26 publications

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“…Preclinical studies that monitor Aβ clearance during sleep using PET radiotracers alongside optical imaging of ISF are needed to corroborate whether Aβ ligands and PET have potential as markers of glymphatic function in the human brain. Future work should also study the extent that elevated ABB in the brain is related to increases in Aβ levels in the peripheral tissue following SD ( 18 , 20 ).…”

Section: Discussionmentioning

confidence: 99%

“…Clinical studies have also shown that Aβ levels in the cerebrospinal fluid (CSF) are the highest before sleep and the lowest after wakening, while CSF Aβ clearance was counteracted by SD ( 16 ). However, there are some inconsistencies between animal models and findings in humans ( 17 ), and Aβ increases in human CSF could reflect factors other than ABB increases in the brain itself ( 18 – 21 ). Notably, the effects of acute SD on Aβ clearance in the human brain have not been documented.…”

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confidence: 99%

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β-Amyloid accumulation in the human brain after one night of sleep deprivation

Shokri‐Kojori

Wang

Wiers

et al. 2018

Proc. Natl. Acad. Sci. U.S.A.

659

397

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SignificanceThere has been an emerging interest in sleep and its association with β-amyloid burden as a risk factor for Alzheimer’s disease. Despite the evidence that acute sleep deprivation elevates β-amyloid levels in mouse interstitial fluid and in human cerebrospinal fluid, not much is known about the impact of sleep deprivation on β-amyloid burden in the human brain. Using positron emission tomography, here we show that acute sleep deprivation impacts β-amyloid burden in brain regions that have been implicated in Alzheimer’s disease. Our observations provide preliminary evidence for the negative effect of sleep deprivation on β-amyloid burden in the human brain.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

β-Amyloid accumulation in the human brain after one night of sleep deprivation

Shokri‐Kojori

Wang

Wiers

et al. 2018

Proc. Natl. Acad. Sci. U.S.A.

659

397

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“…This points to a differential effect on plasma A 40: The time of waking seems to increase A 40, whereas sleep fragmentation, as in our study, does not alter the reduction of A 40 overnight, but specifically seems to diminish the reduction of A 42 overnight. 22 In addition to sleep fragmentation, we carefully controlled for other factors that could influence the A 42, among them on-duty setting, time of demand, and years of professional experience. It is notable that years of professional experience was a significant predictor that diminished the decrease of A 42 in the same direction as sleep fragmenta-…”

Section: F I G U R Ementioning

confidence: 99%

The overnight reduction of amyloid β 1‐42 plasma levels is diminished by the extent of sleep fragmentation, sAPP‐β, and APOE ε4 in psychiatrists on call

Grimmer

Laub

Hapfelmeier

et al. 2020

Alzheimer's & Dementia

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Introduction: In mice there might be an association between sleep deprivation and amyloid plasma levels. Hence, we examined whether amyloid plasma levels are associated with sleep duration or fragmentation in 17 psychiatrists on-call. Methods: Amyloid (A)42, A 40, and soluble amyloid precursor protein (sAPP-) plasma concentrations were measured at the beginning and end of 90 on-call nights, and analyzed using generalized linear models. Results: In on-call nights, a 10.7% reduction of A 42 was revealed overnight. Every single short sleep interruption diminished this reduction by 5.4%, as well as every pg/mL of sAPP-by 1.2%, each copy of APOE 4 by 10.6%, and each year of professional experience by 3.0%. Discussion: The extent of sleep fragmentation diminishes the physiological overnight reduction of A 42 but not A 40 plasma levels in the same direction as the enzyme for A 42 production, the genetic risk factor for Alzheimer's disease (AD), and on-call experience. Might on-call duty and sleep fragmentation in general alter the risk for AD?

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“…A growing number of studies have found that sleep disorders may lead to cognitive impairment and accelerate AD pathology, including increased Aβ deposition in the brain [23]. Our recent studies also showed that sleep deprivation induced peripheral Aβ transport dysfunction in young adults [24], and Aβ accumulation in the brain in rats [25]. The underlying mechanism may involve in the oxidative stress in the brain and plasma [26,27].…”

Section: Discussionmentioning

confidence: 99%

Sleep Disturbance is Associated With Cognitive Impairment: a Community Population-based Cross-sectional Study

Gao¹,

Shan²,

Dang³

et al. 2020

Preprint

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Background: Sleep is an important physiological process and conducive to the elimination of brain metabolites and the recovery of brain function. However, the relationship between sleep disturbance and cognitive impairment is not fully been determined.Methods: This was a community population-based cross-sectional study. A total of 1,461 participants from a village in the suburbs of Xi’an, China were enrolled from January 3 to March 26, 2017. Sleep quality was evaluated using the Pittsburgh sleep quality index (PSQI), and sleep disturbance was defined as a PSQI score >5. Mini-mental state examination (MMSE) was used to assess cognitive function and cognitive impairment was defined as the MMSE score less than cutoff values and meets the diagnostic criteria. Univariate and multivariate analyses were used to analyze the relationships between sleep disturbance and cognitive impairment.Results: Among 1,461 subjects, 87(5.95%) had cognitive impairment, and 842 (57.63%) had sleep disturbance. In bivariate analysis, cognitive impairment was associated with insomnia (ρ=1.000, P＜0.001), age (ρ=0.172, P＜0.001) and educational level (ρ=-0.160, P＜0.001). In the binary logistic regression, cognitive impairment was positively associated with the sleep disturbance (OR=1.779, 95%CI=1.055-3.001, P=0.031). In the internal constitution of PSQI, cognitive impairment was positively associated with the sleep interference (OR=1.678; 95%CI=1.029-2.736, P=0.038), and negatively associated with the habitual sleep efficiency (OR=0.115, 95%CI=0.043-0.306, P<0.001). However, people sleep more than 8 hours a day are more likely to suffer from cognitive impairment (OR=3.174, 95%CI=1.570-6.417, P=0.001). Conclusions: Sleep disturbance is associated with cognitive impairment. However, the causal relationships between sleep disturbances and cognitive impairment are not clear. It needs to be further studied.

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Sleep Deprivation Induced Plasma Amyloid-β Transport Disturbance in Healthy Young Adults

Abstract: Sleep deprivation can lead to an elevation of plasma Aβ40 and decrease of the Aβ42/Aβ40 ratio. The underlying mechanisms may be related to increased oxidative stress and impaired peripheral Aβ clearance as pathomechanisms of AD.

Cited by 50 publications

References 26 publications

β-Amyloid accumulation in the human brain after one night of sleep deprivation

β-Amyloid accumulation in the human brain after one night of sleep deprivation

The overnight reduction of amyloid β 1‐42 plasma levels is diminished by the extent of sleep fragmentation, sAPP‐β, and APOE ε4 in psychiatrists on call

Sleep Disturbance is Associated With Cognitive Impairment: a Community Population-based Cross-sectional Study

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