Changes in the Sleep and Waking EEGs of Nondemented and Demented Elderly Subjects

Journal of the American Geriatrics Society (Impact Factor: 4.22). 03/1982; 30(2):86-93. DOI: 10.1111/j.1532-5415.1982.tb01279.x
Source: PubMed

ABSTRACT 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.

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    • "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.
    Frontiers in Aging Neuroscience 12/2014; 6:325. DOI:10.3389/fnagi.2014.00325 · 2.84 Impact Factor
    • "have also been related to brain dysfunction in the elderly ( Prinz et al . , 1982 ) , and patients diagnosed with probable Alzheimer ' s disease show decreased REM sleep expression compared with age - matched healthy controls ( Reynolds et al . , 1985 ). In rats , REM sleep deprivation contributes to a reduction in hippocampal neurogenesis ( Guzman - Marin et al. , 2008 ) . Although our study did not assess structura"
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    ABSTRACT: Objectives.To investigate the association of mood and anxiety symptoms with sleep architecture (the distribution of sleep stages) in community-dwelling older men.Method.We used in-home unattended polysomnography to measure sleep architecture in older men. Men were categorized into 4 mental health categories: (a) significant depressive symptoms only (DEP+ only, Geriatric Depression Scale ≥ 6), (b) significant anxiety symptoms only (ANX+ only, Goldberg Anxiety Scale ≥ 5), (c) significant depressive and anxiety symptoms (DEP+/ANX+), or (d) no significant depressive or anxiety symptoms (DEP-/ANX-). Compared with men without clinically significant symptomology, men with depressive symptoms spent a higher percentage of time in Stage 2 sleep (65.42% DEP+ only vs 62.47% DEP-/ANX-, p = .003) and a lower percentage of time in rapid eye movement sleep (17.05% DEP+ only vs 19.44% DEP-/ANX-, p = .0005). These differences persisted after adjustment for demographic/lifestyle characteristics, medical conditions, medications, and sleep disturbances, and after excluding participants using psychotropic medications. The sleep architecture of ANX+ or DEP+/ANX+ men did not differ from asymptomatic men.Discussion.Depressed mood in older adults may be associated with accelerated age-related changes in sleep architecture. Longitudinal community-based studies using diagnostic measures are needed to further clarify relationships among common mental disorders, aging, and sleep.
    The Journals of Gerontology Series B Psychological Sciences and Social Sciences 12/2013; DOI:10.1093/geronb/gbt125 · 2.85 Impact Factor
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    • "In AD, sleep latency (the time between going to bed and falling asleep) increases, while total sleep time decreases (Vitiello et al., 1990; Weldemichael and Grossberg, 2010). Patients also experience fragmented sleep with frequent awakenings and longer wake periods during the night (Prinz et al., 1982). Early morning awakenings are also more frequent , as reported by caregivers (McCurry et al., 1999). "
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    ABSTRACT: AD, sleep and circadian rhythm physiology display an intricate relationship. On the one hand, AD pathology leads to sleep and circadian disturbances, with a clear negative influence on quality of life. On the other hand, there is increasing evidence that both sleep and circadian regulating systems exert an influence on AD pathology. In this review we describe the impairments of both sleep regulating systems and circadian rhythms in AD and their link to clinical symptoms, as this may increase knowledge on appropriate diagnosis and adequate treatment of sleep problems in AD. Furthermore we discuss how sleep regulating systems, and especially neurotransmitters such as melatonin and hypocretin, may affect AD pathophysiology, as this may provide a role for lack of sleep and circadian rhythm deterioration in the onset of AD.
    Ageing research reviews 04/2012; 12(1):188-200. DOI:10.1016/j.arr.2012.04.003 · 7.63 Impact Factor
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