Changes in the Sleep and Waking EEGs of Nondemented and Demented Elderly Subjects
Sleep and waking EEGs from 11 healthy nondemented elderly men and from ten inpatients for whom the diagnosis was probable senile dementia of Alzheimer's type (SDAT), were monitored in the subjects' typical home or ward environments or in the sleep laboratory, according to their customary sleep schedules. Aged normal subjects (age range, 56-85 years) had less Stage 3 and Stage 4 sleep, less REM sleep, and more wakefulness than normally observed in young adults. Patients with SDAT (age range, 56-88 years) had even less Stage 3 sleep, no Stage 4 sleep, and very little REM sleep, and experienced fragmentation of their sleep, with frequent awakenings. These sleep variables were significantly different in the SDAT and control groups (MANOVA). Examination of the 24-hour plots of sleep/waking patterns revealed prominent fragmentation of the diurnal sleep/waking rhythm in SDAT patients, with frequent daytime napping and nighttime periods of wakefulness. In addition, significant group differences were observed for the EEG variable, dominant occipital frequency. More qualitative EEG variables (diffuse slowing, spindle activity, and paroxysmal discharges) also differed between groups. It is suggested that correlative neuropathologic data might provide an understanding of the basis for the sleep, EEG, and mental-function factors that undergo change in SDAT.
Available from: Marilyn J Duncan
- "These disturbances include fragmented sleep, frequent nighttime awakenings, and excessive daytime sleepiness (Prinz et al., 1982; Bliwise, 2004; Bliwise et al., 2011). Altered sleep architecture in AD includes reduced rapid eye movement (REM) and slow wave sleep (SWS) in addition to increased latency to REM sleep (Prinz et al., 1982; Bliwise et al., 1989; Perry et al., 1999). Fragmented sleep, which is also common in many other pathological conditions including Parkinson's Disease, Diffuse Lewy Body Disease (DLBD), sleep apnea, and neuromuscular disorders, has wide spread consequences ranging from excessive daytime sleepiness to impaired memory consolidation (Kimoff, 1996; Dauvilliers, 2007; Deschenes and McCurry, 2009; Rolls et al., 2011). "
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ABSTRACT: Sleep perturbations including fragmented sleep with frequent night-time awakenings and daytime naps are common in patients with Alzheimer's disease (AD), and these daily disruptions are a major factor for institutionalization. The objective of this study was to investigate if sleep-wake patterns are altered in 5XFAD mice, a well-characterized double transgenic mouse model of AD which exhibits an early onset of robust AD pathology and memory deficits. These mice have five distinct human mutations in two genes, the amyloid precursor protein (APP) and Presenilin1 (PS1) engineered into two transgenes driven by a neuron specific promoter (Thy1), and thus develop severe amyloid deposition by 4 months of age. Age matched (4-6.5 months old) male and female 5XFAD mice were monitored and compared to wild-type littermate controls for multiple sleep traits using a non-invasive, high throughput, automated piezoelectric system which detects breathing and gross body movements to characterize sleep and wake. Sleep-wake patterns were recorded continuously under baseline conditions (undisturbed) for 3 days and after sleep deprivation of 4 hours, which in mice produces a significant sleep debt and challenge to sleep homeostasis. Under baseline conditions, 5XFAD mice exhibited shorter bout lengths (14% lower values for males and 26% for females) as compared to controls (p<0.001). In females, the 5XFAD mice also showed 12% less total sleep than WT (p<0.01). Bout length reductions were greater during the night (the active phase for mice) than during the day, which does not model the human condition of disrupted sleep at night (the inactive period). However, the overall decrease in bout length suggests increased fragmentation and disruption in sleep consolidation that may be relevant to human sleep. The 5XFAD mice may serve as a useful model for testing therapeutic strategies to improve sleep consolidation in AD patients.
Copyright © 2015. Published by Elsevier Ltd.
Available from: Glenn J Landry
- "However, the directionality of the relationship between sleep and AD has not always been clear. While it is generally accepted that sleep disruptions increase as a function of AD severity (Prinz et al., 1982a,b; Vitiello et al., 1990)—due at least in part to AD-related neuropathology of the circadian system (for review see Coogan et al., 2013)—the role disrupted sleep plays in AD onset and progression has yet to be fully appreciated. Does disrupted sleep somehow cause or accelerate AD? Two recent studies have shed light on this issue: the first provides new evidence showing good sleep quality may be protective "
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ABSTRACT: As of 2010, the worldwide economic impact of dementia was estimated at $604 billion USD; and without discovery of a cure or effective interventions to delay disease progression, dementia’s annual global economic impact is expected to surpass $1 trillion USD as early as 2030. Alzheimer’s disease (AD) is the leading cause of dementia accounting for over 75% of all cases. Toxic accumulation of amyloid beta (Aβ), either by overproduction or some clearance failure, is thought to be an underlying mechanism of the neuronal cell death characteristic of AD—though this amyloid hypothesis has been increasingly challenged in recent years. A compelling alternative hypothesis points to chronic neuroinflammation as a common root in late-life degenerative diseases including AD. Apolipoprotein-E (APOE) genotype is the strongest genetic risk factor for AD: APOE-ε4 is proinflammatory and individuals with this genotype accumulate more Aβ, are at high risk of developing AD, and almost half of all AD patients have at least one ε4 allele. Recent studies suggest a bidirectional relationship exists between sleep and AD pathology. Sleep may play an important role in Aβ clearance, and getting good quality sleep vs. poor quality sleep might reduce the AD risk associated with neuroinflammation and the ε4 allele. Taken together, these findings are particularly important given the sleep disruptions commonly associated with AD and the increased burden disrupted sleep poses for AD caregivers. The current review aims to: (1) identify individuals at high risk for dementia who may benefit most from sleep interventions; (2) explore the role poor sleep quality plays in exacerbating AD type dementia; (3) examine the science of sleep interventions to date; and (4) provide a road map in pursuit of comprehensive sleep interventions, specifically targeted to promote cognitive function and delay progression of dementia.
- "While mean REM sleep episode duration is decreased, the total number of REM sleep episodes and REM sleep latency remain intact . EEG slowing during REM sleep has been proposed to be a biological marker of AD . Hassainia et al. observed an increase in absolute delta and theta activities, and a decrease in absolute alpha and beta activities during REM sleep in AD, those alterations affecting particularly the parietotemporal and frontal regions . "
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ABSTRACT: Sleep disorders are frequent in Alzheimer's disease (AD), with a significant impact on patients and caregivers and a major risk factor for early institutionalization. Micro-architectural sleep alterations, nocturnal sleep fragmentation, decrease in nocturnal sleep duration, diurnal napping and even inversion of the sleep-wake cycle are the main disorders observed in patients with AD. Experimental and epidemiological evidence for a close reciprocal interaction between cognitive decline and sleep alterations is growing. Management of sleep disorders in AD is pre-eminently behavioral. Association of melatonin and bright light treatment seems to be promising as well. The presence of sleep complaints, especially excessive somnolence in demented patients, should draw attention to possible associated sleep pathologies such as sleep apnea syndrome or restless legs syndrome.
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