Sleep Quality and Preclinical Alzheimer Disease

Ju, Yo‐El; McLeland, Jennifer; Toedebusch, Cristina D.; Xiong, Chengjie; Fagan, Anne M.; Duntley, Stephen P.; Morris, John C.; Holtzman, David M.

doi:10.1001/jamaneurol.2013.2334

Cited by 602 publications

(587 citation statements)

References 39 publications

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“…Classical hallmarks of AD are insoluble extracellular senile plaques composed of the http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=4865 (Aβ) peptide and intracellular tangles comprising hyper‐phosphorylated τ aggregates (Perrin et al, 2009). Aβ plaques accumulate in the brains of AD patients' years before the onset of cognitive impairment and serve as an early biomarker of AD (Ju et al, 2013). …”

Section: Melatonin In the Treatment Of Circadian Rhythm And Sleep Dismentioning

confidence: 99%

“…Importantly, Aβ overlaps DMN regions in which hypometabolism and atrophy were detected in AD patients (Buckner et al, 2005). Aβ deposition in the preclinical stage of AD appears to be associated with worse sleep quality (Ju et al, 2013; Spira and Gottesman, 2017) and was also associated with worse cognitive and memory performance (Molano et al, 2017). An alternative mechanism linking sleep and Aβ has been recently suggested (Mendelsohn and Larrick, 2013), whereby sleep can facilitate the removal of toxic proteins and other molecules from the brain through regulation of the ‘glymphatic’ system (Jessen et al, 2015).…”

Section: Melatonin In the Treatment Of Circadian Rhythm And Sleep Dismentioning

confidence: 99%

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New perspectives on the role of melatonin in human sleep, circadian rhythms and their regulation

Zisapel

2018

British J Pharmacology

545

350

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In mammals, a central circadian clock, located in the suprachiasmatic nuclei (SCN) of the hypothalamus, tunes the innate circadian physiological rhythms to the ambient 24 h light–dark cycle to invigorate and optimize the internal temporal order. The SCN‐activated, light‐inhibited production of melatonin conveys the message of darkness to the clock and induces night‐state physiological functions, for example, sleep/wake blood pressure and metabolism. Clinically meaningful effects of melatonin treatment have been demonstrated in placebo‐controlled trials in humans, particularly in disorders associated with diminished or misaligned melatonin rhythms, for example, circadian rhythm‐related sleep disorders, jet lag and shift work, insomnia in children with neurodevelopmental disorders, poor (non‐restorative) sleep quality, non‐dipping nocturnal blood pressure (nocturnal hypertension) and Alzheimer's disease (AD). The diminished production of melatonin at the very early stages of AD, the role of melatonin in the restorative value of sleep (perceived sleep quality) and its sleep‐anticipating effects resulting in attenuated activation of certain brain networks are gaining a new perspective as the role of poor sleep quality in the build‐up of β amyloid, particularly in the precuneus, is unravelled. As a result of the recently discovered relationship between circadian clock, sleep and neurodegeneration, new prospects of using melatonin for early intervention, to promote healthy physical and mental ageing, are of prime interest in view of the emerging link to the aetiology of Alzheimer's disease.Linked ArticlesThis article is part of a themed section on Recent Developments in Research of Melatonin and its Potential Therapeutic Applications. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v175.16/issuetoc

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Section: Melatonin In the Treatment Of Circadian Rhythm And Sleep Dismentioning

confidence: 99%

Section: Melatonin In the Treatment Of Circadian Rhythm And Sleep Dismentioning

confidence: 99%

New perspectives on the role of melatonin in human sleep, circadian rhythms and their regulation

Zisapel

2018

British J Pharmacology

545

350

View full text Add to dashboard Cite

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“…Another cross-sectional study of 142 cognitively normal middle-aged and older adults showed that lower CSF Aβ42 levels, which indicate greater Aβ deposition, were associated with Manuscript number: 16-1287R2 5 poorer actigraphic measured sleep efficiency and higher frequency of waking episodes after sleep onset (WASO) [31]. However, despite evidence from these cross-sectional studies, it remains difficult to infer with certainty that poor sleep is a contributor to AD pathogenesis.…”

Section: Associations Between Sleep Disruption and Admentioning

confidence: 99%

Is Sleep Disruption a Risk Factor for Alzheimer’s Disease?

Macedo

Balouch

Tabet

2017

JAD

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Sleep disturbances are routinely encountered in Alzheimer's disease (AD) and affect about 25-40% of patients in the mild-to-moderate stages of the disease. In many, sleep pathology may represent a symptom of the underlying neurodegeneration. However, a history of sleep disruption occurring years prior to onset of cognitive symptoms could represent a potential risk factor for AD. The aim of the present narrative review was to evaluate current evidence linking sleep disturbances with AD development and to understand the mechanisms that may contribute to this.Although the mechanisms by which poor sleep may contribute to AD genesis is not fully understood, emerging evidence linking disturbances in the sleep wake cycle with Aβ deposition is shedding light on the relationship between sleep pathology and the subsequent development of AD. Aβ burden appears to be enhanced by sleep-wake cycle disruptions and is suspected as being an important mechanism by which sleep disruptions contribute in AD development. Other mechanisms triggered by sleep disruption may also be involved in AD development, such as brain hypoxia, oxidative stress, circadian activity rhythms disturbances, overexpression of orexins and blood brain barrier impairment. Further understanding of the link between sleep disturbances and future development of AD is still needed before sleep disturbances are clearly marked as a preventable risk factor for AD. In these circumstances, early lifestyle interventions to help increase the quantity and quality of sleep may have a favorable outcome on decreasing the incidence of AD and this needs to be investigated further.

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“…[3][4][5][6] For example, rapid eye movement (REM) sleep behavior disorder (RBD) may precede the development of a synucleinopathy by decades, [7][8][9][10] and reduced sleep efficiency is seen in patients with preclinical AD. 11 Furthermore, increasing evidence shows that sleep disruption can accelerate neurodegenerative processes including toxic protein aggregation in preclinical models, and increases the risk of developing symptomatic AD. 4,[11][12][13] Therefore, understanding the relationship between sleep pathology and CJD may enhance our understanding of the bidirectional relationship between sleep and other common neurodegenerative processes.…”

Section: Introductionmentioning

confidence: 99%

“…11 Furthermore, increasing evidence shows that sleep disruption can accelerate neurodegenerative processes including toxic protein aggregation in preclinical models, and increases the risk of developing symptomatic AD. 4,[11][12][13] Therefore, understanding the relationship between sleep pathology and CJD may enhance our understanding of the bidirectional relationship between sleep and other common neurodegenerative processes. Although sleep symptoms have not been traditionally viewed as a cardinal symptom of CJD, sleep-wake disturbances are a significant source of morbidity and adversely affect quality of life in these patients.…”

Section: Introductionmentioning

confidence: 99%

Sleep Pathology in Creutzfeldt-Jakob Disease

Kang

Bruin

Wang

et al. 2016

Journal of Clinical Sleep Medicine

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Study Objectives: Associations between sleep and neurodegenerative diseases have become increasingly evident. This study aims to characterize the prevalence and type of sleep pathology in Creutzfeldt-Jakob disease (CJD), a rapidly progressive, fatal neurodegenerative disease. Methods: In this observational cross-sectional cohort study, we performed a retrospective analysis of sleep signs and symptoms in a consecutive group of patients with definite CJD at a tertiary care medical center (n = 28). Polysomnography was performed in 14 patients. Results: Although only 5 of 28 patients carried a premorbid sleep diagnosis, signs/symptoms of sleep pathology were present in 25 patients. Eleven reported hypersomnia whereas 13 reported insomnia. Seven had restless legs symptoms and/or periodic limb movements of sleep, and nine reported parasomnias. Of the 14 patients who underwent polysomnography, 1 did not show sleep, 9 (69%) had poorly formed or absent sleep spindles and/or K-complexes, and 10 (77%) had sleep-disordered breathing. Of the 8 patients who experienced rapid eye movement (REM) sleep during the polysomnography, 3 (38%) showed REM sleep without atonia, and 2 patients met criteria for REM sleep behavior disorder. Median total sleep time was 226 (interquartile range [IQR] = 195-282) min. Median sleep efficiency was 58.5% (IQR = 41-65.5 %). Median REM time was 0.35% (IQR = 0-7.125%). Five patients (38%) demonstrated periodic limb movements during polysomnography. One case is presented. Conclusions: Sleep pathology is common in CJD, and screening for sleep pathology is indicated in the evaluation of patients with rapidly progressive dementias. Early identification and treatment of sleep pathology may provide an intervenable target for CJD.

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Sleep Quality and Preclinical Alzheimer Disease

Cited by 602 publications

References 39 publications

New perspectives on the role of melatonin in human sleep, circadian rhythms and their regulation

New perspectives on the role of melatonin in human sleep, circadian rhythms and their regulation

Is Sleep Disruption a Risk Factor for Alzheimer’s Disease?

Sleep Pathology in Creutzfeldt-Jakob Disease

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