Obstructive sleep apnea treatment, slow wave activity, and amyloid‐β

Ju, Yo‐El; Zangrilli, Margaret A.; Finn, Mary Beth; Fagan, Anne M.; Holtzman, David M.

doi:10.1002/ana.25408

Cited by 79 publications

(54 citation statements)

References 19 publications

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“…Moreover, one recent study indicated that consecutive nights of partial sleep deprivation, with preserved SWS, had no effect on CSF biomarkers for amyloid deposition, neuronal injury, and astroglial activation 40 . More recently, it was shown that OSA treatment increased slow wave activity (SWA) and that SWA was significantly correlated with lower Aβ after treatment 41 . Altogether, these lines of evidence have demonstrated that management of NREM SWS might be a promising target for AD prevention.…”

Section: Discussionmentioning

confidence: 99%

Sleep characteristics and cerebrospinal fluid biomarkers of Alzheimer's disease pathology in cognitively intact older adults: The CABLE study

Tan

et al. 2020

Alzheimer's & Dementia

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Introduction This study tested the self‐reported sleep characteristics associated with cerebrospinal fluid (CSF) Alzheimer's disease (AD) biomarkers in cognitively intact older adults. Methods The linear and non‐linear regression analyses were conducted in 736 cognitively normal participants (mean [standard deviation; SD] age, 62.3 [10.5] years, range 40 to 88 years, 59% female) who had measurements of cerebrospinal fluid (CSF) amyloid beta (Aβ) and tTau proteins and sleep characteristics, after adjusting for age, gender, education, apolipoprotein E gene (APOE) ε4 status, and general cognition. Results Greater daytime sleepiness was associated with higher CSF indicators of amyloid deposition in female patients. No significant associations were revealed for CSF tTau proteins after Bonferroni correction. A U‐shaped relationship was revealed for nocturnal sleep habits, such that those with insufficient or excessive nocturnal sleep duration had greater CSF biomarkers of amyloid deposition (the reflection range: bedtime: around 10:00 p.m. and sleep duration: 6.0 to 6.5 hours). Discussion These findings consolidated the close relationship between sleep and AD.

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Section: Discussionmentioning

confidence: 99%

Sleep characteristics and cerebrospinal fluid biomarkers of Alzheimer's disease pathology in cognitively intact older adults: The CABLE study

Tan

et al. 2020

Alzheimer's & Dementia

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“…Conversely, patients with OSA obtained worse results in neuropsychological tests of executive functions, such as attention and memory. Importantly, patients with OSA carrying at least one APOEε4 allele, and therefore at risk of develop AD, presented lower scores than those with OSA that do not carry the gene [93]. In this regard, a prospective study with cognitively normal older women showed that those with severe sleep breathing disorder had an increased risk of developing MCI or dementia at follow-up [47].…”

Section: Mechanisms Linking Sleep Respiratory Disorders With Admentioning

confidence: 99%

“…It was associated with sleep fragmentation, daytime sleepiness and significant cardiovascular and metabolic disturbances. Furthermore, OSA might be a risk factor for developing MCI and dementia in the aging population, as it induced cognitive dysfunction in many domains, such as attention, episodic memory, working memory, and executive function [93].…”

Section: Mechanisms Linking Sleep Respiratory Disorders With Admentioning

confidence: 99%

Is Sleep Disruption a Cause or Consequence of Alzheimer’s Disease? Reviewing Its Possible Role as a Biomarker

Lloret

Cervera‐Ferri

Nepomuceno

et al. 2020

IJMS

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In recent years, the idea that sleep is critical for cognitive processing has gained strength. Alzheimer's disease (AD) is the most common form of dementia worldwide and presents a high prevalence of sleep disturbances. However, it is difficult to establish causal relations, since a vicious circle emerges between different aspects of the disease. Nowadays, we know that sleep is crucial to consolidate memory and to remove the excess of beta-amyloid and hyperphosphorilated tau accumulated in AD patients' brains. In this review, we discuss how sleep disturbances often precede in years some pathological traits, as well as cognitive decline, in AD. We describe the relevance of sleep to memory consolidation, focusing on changes in sleep patterns in AD in contrast to normal aging. We also analyze whether sleep alterations could be useful biomarkers to predict the risk of developing AD and we compile some sleep-related proposed biomarkers. The relevance of the analysis of the sleep microstructure is highlighted to detect specific oscillatory patterns that could be useful as AD biomarkers.the risk of developing AD [9]. Similarly, Bubu and colleagues estimated in a meta-analysis that the risk of dementia in patients with sleep disorders was 1.68 times greater [10]. Moreover, in a recent multi-center study, both midlife and late-life terminal insomnia were associated with a higher risk of dementia [11].It is interesting to note that affected brain structures in people with disturbed sleep coincide with vulnerable areas in AD. Lower gray matter volume in hippocampus, precuneus, amygdala, and cingulate gyrus [12][13][14][15][16][17][18][19], and a higher degree of cortical atrophy have been described in cognitively-unimpaired insomnia patients [14,20]. A recent study performed in cognitively unimpaired adults aged between 45 and 75, found that insomnia patients presented decreases in grey matter volume in AD-related areas, that concur with other studies. Furthermore, they found greater volume in the left caudate in these subjects, which can also be seen in presymptomatic carriers of an AD genetic mutation [21]. Finally, a very recent study in middle-aged, cognitively unimpaired adults found lower grey matter volumes in the left angular gyrus, the bilateral superior frontal gyri, the thalami, and the right hippocampus in insomniac APOE-ε4 carriers (AD's main risk factor) when compared to non-carriers with or without insomnia [21].This temporal and anatomical relationship could suggest that sleep disturbances may influence or exacerbate AD pathology and that improving sleep may help slow down its progression [22,23]. Additionally, sleep alterations could be used to predict the risk of developing dementia and could also serve as early indicators of the disease. If sleep disorders constitute a risk factor to initiate or to accelerate the clinical course of AD, they could be used to develop disease biomarkers. Furthermore, a sleep biomarker with high sensitivity and specificity would be extremely useful, as electrophysiological re...

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“…In our study, we sought to isolate the effects of obstructive sleep apnea treatment on cerebrospinal fluid (CSF) amyloid‐β (Aβ) from other factors that influence soluble Aβ levels. Most importantly, amyloid plaques are associated with decreased CSF Aβ, particularly Aβ42, due to a probable “sink” effect, whether in symptomatic Alzheimer disease (AD) or during the asymptomatic preclinical phase of AD .…”

mentioning

confidence: 99%

Obstructive sleep apnea treatment, slow wave activity, and amyloid‐β

Cited by 79 publications

References 19 publications

Sleep characteristics and cerebrospinal fluid biomarkers of Alzheimer's disease pathology in cognitively intact older adults: The CABLE study

Sleep characteristics and cerebrospinal fluid biomarkers of Alzheimer's disease pathology in cognitively intact older adults: The CABLE study

Is Sleep Disruption a Cause or Consequence of Alzheimer’s Disease? Reviewing Its Possible Role as a Biomarker

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