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

Shokri‐Kojori, Ehsan; Wang, Gene‐Jack; Wiers, Corinde E.; Demiral, Şükrü Barış; Guo, Min; Kim, Sung Won; Lindgren, Elsa; Ramirez, Veronica; Zehra, Amna; Freeman, Clara; Miller, Gregg; Manza, Peter; Srivastava, Tansha; Santi, Susan De; Tomasi, Dardo; Benveniste, Helene; Volkow, Nora D.

doi:10.1073/pnas.1721694115

Cited by 660 publications

(455 citation statements)

References 71 publications

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“…Sleep disturbance and insomnia are common in Alzheimer's disease (AD), affecting ≈40% of patients . There is emerging evidence that poor sleep may contribute to the development of AD and impair memory function . Options for effective pharmacological treatment of insomnia in AD are limited, with inconsistent or poor‐quality evidence for efficacy of melatonin, second‐generation antipsychotics (which are primarily used to target other neuropsychiatric and behavioral symptoms associated with AD), and sedating antidepressants .…”

Section: Introductionmentioning

confidence: 99%

“…1 There is emerging evidence that poor sleep may contribute to the development of AD and impair memory function. [2][3][4][5][6][7][8][9] Options for effective pharmacological treatment of insomnia in AD are limited, with inconsistent or poor-quality evidence for efficacy of melatonin, [10][11][12][13] second-generation antipsychotics (which are primarily used to target other neuropsychiatric…”

Section: Introductionmentioning

confidence: 99%

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Polysomnographic assessment of suvorexant in patients with probable Alzheimer's disease dementia and insomnia: a randomized trial

Herring

Ceesay

Snyder

et al. 2020

Alzheimer's & Dementia

129

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Introduction We evaluated the clinical profile of the orexin receptor antagonist suvorexant for treating insomnia in patients with mild‐to‐moderate probable Alzheimer's disease (AD) dementia. Methods Randomized, double‐blind, 4‐week trial of suvorexant 10 mg (could be increased to 20 mg based on clinical response) or placebo in patients who met clinical diagnostic criteria for both probable AD dementia and insomnia. Sleep was assessed by overnight polysomnography in a sleep laboratory. The primary endpoint was change‐from‐baseline in polysomnography‐derived total sleep time (TST) at week 4. Results Of 285 participants randomized (suvorexant, N = 142; placebo, N = 143), 277 (97%) completed the trial (suvorexant, N = 136; placebo, N = 141). At week 4, the model‐based least squares mean improvement‐from‐baseline in TST was 73 minutes for suvorexant and 45 minutes for placebo; (difference = 28 minutes [95% confidence interval 11‐45], p < 0.01). Somnolence was reported in 4.2% of suvorexant‐treated patients and 1.4% of placebo‐treated patients. Discussion Suvorexant improved TST in patients with probable AD dementia and insomnia.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Polysomnographic assessment of suvorexant in patients with probable Alzheimer's disease dementia and insomnia: a randomized trial

Herring

Ceesay

Snyder

et al. 2020

Alzheimer's & Dementia

129

View full text Add to dashboard Cite

show abstract

“…The relationship between sleep and Aβ appears reciprocal, as Aβ increase after sleep deprivation 65 , while Aβ accumulation in turn increases wakefulness and alters sleep patterns 66 . Here, although Aβ status did not relate to sleep efficiency or hippocampus decline alone, the sleep-hippocampal decline relationship was significantly stronger in the Aβ positive participants.…”

Section: Discussionmentioning

confidence: 99%

Self-Reported Sleep Relates to Microstructural Hippocampal Decline in β-Amyloid Positive Adults Beyond Genetic Risk

Grydeland

Sederevičius

Wang

et al. 2020

Preprint

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Objective:To test the hypothesis that worse self-reported sleep relates to reduced hippocampal integrity as indexed by increased intra-hippocampal water diffusion, and that this relationship is stronger in the presence of β-amyloid (Aβ) accumulation, a marker of Alzheimer's disease (AD) pathology. Methods. Two-hundred and fifty-one participants, aged 19-81 years, completed the Pittsburgh Sleep Quality Index, and 2 diffusion tensor imaging sessions, on average 3 years apart, allowing estimates of decline in hippocampal microstructural integrity as indexed by increased mean diffusivity (MD). We used the delayed recall from the California Verbal Learning Test to measure memory change. 18 F-Flutemetamol PET, in 108 participants above 44 years of age, yielded 23 Aβ positive cases. Genotyping enabled controlling for APOE ε4 status, and polygenic scores for sleep efficiency and AD. Results. Worse global sleep quality and sleep efficiency related to more rapid reduction in hippocampal microstructural integrity over time. Focusing on sleep efficiency, this relationship was stronger in presence of cortical Aβ accumulation. Sleep efficiency also related to memory decline indirectly via hippocampal integrity decline. The results were not explained by genetic risk for sleep efficiency and AD. Conclusions. Poor self-reported sleep efficiency related to decline in hippocampal integrity, especially in the presence of Aβ accumulation. Poor sleep and hippocampal microstructural decline may partly explain memory decline in older adults with Aβ pathology. The relationships were not explained by genetic risk, and poor selfreported sleep efficiency might constitute a risk factor for AD, although the causal mechanisms driving the of observed associations are unknown.

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“…Increased levels of intracerebral tau and ß-amyloid have been observed in healthy adults after sleep loss (11,12), and recently sleep driven parenchymal CSF pulsations in the fourth ventricle were demonstrated in the human brain (13), providing the first evidence for human glymphatic mechanisms. To date, however, no studies have described the link between AQP4 and human sleep-wake regulation or investigated whether genetic modulation of AQP4 may have restorative effects on cognitive functions after sleep loss.…”

Section: Introductionmentioning

confidence: 98%

Haplotype of the astrocytic water channel AQP4 modulates slow wave energy in human NREM sleep

Smu

Landolt

Berger

et al. 2019

Preprint

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Cerebrospinal fluid (CSF) flow through the brain parenchyma is facilitated by the astrocytic water channel aquaporin 4 (AQP4). Homeostatically regulated electroencephalographic (EEG) slow waves are a hallmark of deep non-rapid-eye-movement (NREM) sleep and have been implicated in the regulation of parenchymal CSF flow and brain clearance. The human AQP4 gene harbors several single nucleotide polymorphisms (SNPs) associated with AQP4 expression, brain-water homeostasis and neurodegenerative diseases. To date, their role in sleep-wake regulation is unknown. To investigate whether functional variants in AQP4 modulate human sleep, nocturnal EEG-recordings and cognitive performance were investigated in 123 healthy participants genotyped for a common eight-SNP AQP4-haplotype. We show that this AQP4-haplotype is associated with distinct modulations of NREM slow wave energy, strongest in early sleep and mirrored by changes in sleepiness and reaction times during extended wakefulness. The study provides the first human evidence for a link between AQP4, deep NREM sleep and cognitive consequences of prolonged wakefulness.

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

Cited by 660 publications

References 71 publications

Polysomnographic assessment of suvorexant in patients with probable Alzheimer's disease dementia and insomnia: a randomized trial

Polysomnographic assessment of suvorexant in patients with probable Alzheimer's disease dementia and insomnia: a randomized trial

Self-Reported Sleep Relates to Microstructural Hippocampal Decline in β-Amyloid Positive Adults Beyond Genetic Risk

Haplotype of the astrocytic water channel AQP4 modulates slow wave energy in human NREM sleep

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