FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2605277320> ?p ?o ?g. }

• W2605277320 endingPage "36" @default.
• W2605277320 startingPage "19" @default.
• W2605277320 abstract "Older adults do not sleep as well as younger adults. Why? What alterations in sleep quantity and quality occur as we age, and are there functional consequences? What are the underlying neural mechanisms that explain age-related sleep disruption? This review tackles these questions. First, we describe canonical changes in human sleep quantity and quality in cognitively normal older adults. Second, we explore the underlying neurobiological mechanisms that may account for these human sleep alterations. Third, we consider the functional consequences of age-related sleep disruption, focusing on memory impairment as an exemplar. We conclude with a discussion of a still-debated question: do older adults simply need less sleep, or rather, are they unable to generate the sleep that they still need? Older adults do not sleep as well as younger adults. Why? What alterations in sleep quantity and quality occur as we age, and are there functional consequences? What are the underlying neural mechanisms that explain age-related sleep disruption? This review tackles these questions. First, we describe canonical changes in human sleep quantity and quality in cognitively normal older adults. Second, we explore the underlying neurobiological mechanisms that may account for these human sleep alterations. Third, we consider the functional consequences of age-related sleep disruption, focusing on memory impairment as an exemplar. We conclude with a discussion of a still-debated question: do older adults simply need less sleep, or rather, are they unable to generate the sleep that they still need? Normative aging is associated with a reduced ability to initiate and maintain sleep. Moreover, deficits in sleep physiology, including those of non-rapid eye movement (NREM) sleep and its associated neural oscillations, are especially prominent in later life. Though sleep disruption is a common signature of “normal aging”, the underlying neural mechanisms explaining age-related sleep impairment are only now being revealed. This review focuses on physiological changes associated with normative human aging. First, we characterize associated alterations in sleep structure and oscillatory activity in later life. Second, we describe emerging neurobiological mechanisms that may account for these sleep alterations. Third, we consider the functional consequences of age-related sleep disruption, focusing on memory impairment. We conclude with the exploration of a still-unresolved question: are older adults unable to generate the sleep that they need or do they simply need sleep less. Both the macro-level structure of sleep, such as sleep duration and sleep stages, and the micro-level architecture of sleep, including the quantity and quality of sleep oscillations, change as we progress into our older age. Advancing into the fifth decade of older age and beyond are a collection of well-characterized changes in sleep architecture (Figure 1A): (1) advanced sleep timing (i.e., earlier bedtimes and rise times), (2) longer sleep-onset latency (i.e., longer time taken to fall asleep), (3) shorter overall sleep duration, (4) increased sleep fragmentation (i.e., less consolidated sleep with more awakenings, arousals, or transitions to lighter sleep stages), (5) more fragile sleep (i.e., higher likelihood of being woken by external sensory stimuli), (6) reduced amount of deeper NREM sleep known as slow wave sleep (SWS), (7) increased time spent in lighter NREM stages 1 and 2, (8) shorter and fewer NREM-REM sleep cycles, and (9) increased time spent awake throughout the night (Conte et al., 2014Conte F. Arzilli C. Errico B.M. Giganti F. Iovino D. Ficca G. Sleep measures expressing ‘functional uncertainty’ in elderlies’ sleep.Gerontology. 2014; 60: 448-457Crossref PubMed Scopus (1) Google Scholar, Feinberg and Carlson, 1968Feinberg I. Carlson V.R. Sleep variables as a function of age in man.Arch. Gen. Psychiatry. 1968; 18: 239-250Crossref Scopus (0) Google Scholar, Kales et al., 1967Kales A. Wilson T. Kales J.D. Jacobson A. Paulson M.J. Kollar E. Walter R.D. Measurements of all-night sleep in normal elderly persons: effects of aging.J. Am. Geriatr. Soc. 1967; 15: 405-414Crossref PubMed Scopus (85) Google Scholar, Klerman and Dijk, 2008Klerman E.B. Dijk D.J. Age-related reduction in the maximal capacity for sleep--implications for insomnia.Curr. Biol. 2008; 18: 1118-1123Abstract Full Text Full Text PDF PubMed Scopus (0) Google Scholar, Landolt et al., 1996Landolt H.P. Dijk D.J. Achermann P. Borbély A.A. Effect of age on the sleep EEG: slow-wave activity and spindle frequency activity in young and middle-aged men.Brain Res. 1996; 738: 205-212Crossref PubMed Scopus (183) Google Scholar, Ohayon et al., 2004Ohayon M.M. Carskadon M.A. Guilleminault C. Vitiello M.V. Meta-analysis of quantitative sleep parameters from childhood to old age in healthy individuals: developing normative sleep values across the human lifespan.Sleep. 2004; 27: 1255-1273Crossref PubMed Scopus (1723) Google Scholar, Redline et al., 2004Redline S. Kirchner H.L. Quan S.F. Gottlieb D.J. Kapur V. Newman A. The effects of age, sex, ethnicity, and sleep-disordered breathing on sleep architecture.Arch. Intern. Med. 2004; 164: 406-418Crossref PubMed Scopus (306) Google Scholar, Van Cauter et al., 2000Van Cauter E. Leproult R. Plat L. Age-related changes in slow wave sleep and REM sleep and relationship with growth hormone and cortisol levels in healthy men.JAMA. 2000; 284: 861-868Crossref PubMed Google Scholar, Vienne et al., 2016Vienne J. Spann R. Guo F. Rosbash M. Age-related reduction of recovery sleep and arousal threshold in Drosophila.Sleep. 2016; 39: 1613-1624Crossref PubMed Scopus (3) Google Scholar, Webb and Campbell, 1979Webb W.B. Campbell S.S. The first night effect revisited with age as a variable.Waking Sleeping. 1979; 3: 319-324PubMed Google Scholar, Zepelin et al., 1984Zepelin H. McDonald C.S. Zammit G.K. Effects of age on auditory awakening thresholds.J. Gerontol. 1984; 39: 294-300Crossref PubMed Google Scholar). This is not to suggest a lack of individual variability in the degree of sleep disruption. It is clear that some older adults show little sleep impairment, while others show dramatic alterations, despite chronological age being similar (Redline et al., 2004Redline S. Kirchner H.L. Quan S.F. Gottlieb D.J. Kapur V. Newman A. The effects of age, sex, ethnicity, and sleep-disordered breathing on sleep architecture.Arch. Intern. Med. 2004; 164: 406-418Crossref PubMed Scopus (306) Google Scholar, Vitiello, 2009Vitiello M.V. Recent advances in understanding sleep and sleep disturbances in older adults: growing older does not mean sleeping poorly.Curr. Dir. Psychol. Sci. 2009; 18: 316-320Crossref Scopus (0) Google Scholar), a topic that we will return to throughout this review. Though age-related reductions in REM sleep time have been reported, these are subtler relative to changes in NREM sleep. Often, REM sleep impairments only emerge as adults progress into their 80s and beyond (Ohayon et al., 2004Ohayon M.M. Carskadon M.A. Guilleminault C. Vitiello M.V. Meta-analysis of quantitative sleep parameters from childhood to old age in healthy individuals: developing normative sleep values across the human lifespan.Sleep. 2004; 27: 1255-1273Crossref PubMed Scopus (1723) Google Scholar, Van Cauter et al., 2000Van Cauter E. Leproult R. Plat L. Age-related changes in slow wave sleep and REM sleep and relationship with growth hormone and cortisol levels in healthy men.JAMA. 2000; 284: 861-868Crossref PubMed Google Scholar) or as a symptom of degenerative dementias (Brayet et al., 2015Brayet P. Petit D. Frauscher B. Gagnon J.F. Gosselin N. Gagnon K. Rouleau I. Montplaisir J. Quantitative EEG of rapid-eye-movement sleep: A marker of amnestic mild cognitive impairment.Clin. EEG Neurosci. 2015; 47: 134-141Crossref PubMed Scopus (2) Google Scholar, Hita-Yañez et al., 2012Hita-Yañez E. Atienza M. Gil-Neciga E. Cantero J.L. Disturbed sleep patterns in elders with mild cognitive impairment: the role of memory decline and ApoE ε4 genotype.Curr. Alzheimer Res. 2012; 9: 290-297Crossref PubMed Scopus (28) Google Scholar, Petit et al., 2004Petit D. Gagnon J.F. Fantini M.L. Ferini-Strambi L. Montplaisir J. Sleep and quantitative EEG in neurodegenerative disorders.J. Psychosom. Res. 2004; 56: 487-496Abstract Full Text Full Text PDF PubMed Scopus (161) Google Scholar) (discussed in Box 1) .Box 1Sleep, Neuropathology, and Abnormal AgingBeyond normative aging, sleep disruption is especially pervasive in neurodegenerative dementias. To date, the majority of pathological evidence concerns β-amyloid (Aβ) protein and tau neurofibrillary tangles that are characteristic of Alzheimer’s disease (AD). Subjective and objective measures of poor sleep correlate with cortical Aβ burden, as well as cerebrospinal fluid measures of Aβ and phosphorylated tau (Liguori et al., 2014Liguori C. Romigi A. Nuccetelli M. Zannino S. Sancesario G. Martorana A. Albanese M. Mercuri N.B. Izzi F. Bernardini S. et al.Orexinergic system dysregulation, sleep impairment, and cognitive decline in Alzheimer disease.JAMA Neurol. 2014; 71: 1498-1505Crossref PubMed Scopus (48) Google Scholar, Mander et al., 2015Mander B.A. Marks S.M. Vogel J.W. Rao V. Lu B. Saletin J.M. Ancoli-Israel S. Jagust W.J. Walker M.P. β-amyloid disrupts human NREM slow waves and related hippocampus-dependent memory consolidation.Nat. Neurosci. 2015; 18: 1051-1057Crossref PubMed Scopus (75) Google Scholar, Spira et al., 2013Spira A.P. Gamaldo A.A. An Y. Wu M.N. Simonsick E.M. Bilgel M. Zhou Y. Wong D.F. Ferrucci L. Resnick S.M. Self-reported sleep and β-amyloid deposition in community-dwelling older adults.JAMA Neurol. 2013; 70: 1537-1543Crossref PubMed Scopus (114) Google Scholar, Sprecher et al., 2015Sprecher K.E. Bendlin B.B. Racine A.M. Okonkwo O.C. Christian B.T. Koscik R.L. Sager M.A. Asthana S. Johnson S.C. Benca R.M. Amyloid burden is associated with self-reported sleep in nondemented late middle-aged adults.Neurobiol. Aging. 2015; 36: 2568-2576Abstract Full Text Full Text PDF PubMed Scopus (32) Google Scholar). Similar associations have been observed in animals, with Aβ accumulation in rodent models of AD predicting greater sleep fragmentation (Roh et al., 2012Roh J.H. Huang Y. Bero A.W. Kasten T. Stewart F.R. Bateman R.J. Holtzman D.M. Disruption of the sleep-wake cycle and diurnal fluctuation of β-amyloid in mice with Alzheimer’s disease pathology.Sci. Transl. Med. 2012; 4: 150ra122Crossref PubMed Scopus (133) Google Scholar). Recent studies in humans have further established that Aβ is selectively associated with the loss of <1 Hz NREM sleep oscillations (Mander et al., 2015Mander B.A. Marks S.M. Vogel J.W. Rao V. Lu B. Saletin J.M. Ancoli-Israel S. Jagust W.J. Walker M.P. β-amyloid disrupts human NREM slow waves and related hippocampus-dependent memory consolidation.Nat. Neurosci. 2015; 18: 1051-1057Crossref PubMed Scopus (75) Google Scholar). This association between Aβ and <1 Hz NREM oscillations appears to be unique and distinct from general age-related reductions in the broader SWA range of 0.6–4.8 Hz; with the latter linked, instead, to gray matter atrophy within the medial prefrontal cortex (Dubé et al., 2015Dubé J. Lafortune M. Bedetti C. Bouchard M. Gagnon J.F. Doyon J. Evans A.C. Lina J.M. Carrier J. Cortical thinning explains changes in sleep slow waves during adulthood.J. Neurosci. 2015; 35: 7795-7807Crossref PubMed Scopus (5) Google Scholar, Mander et al., 2013Mander B.A. Rao V. Lu B. Saletin J.M. Lindquist J.R. Ancoli-Israel S. Jagust W. Walker M.P. Prefrontal atrophy, disrupted NREM slow waves and impaired hippocampal-dependent memory in aging.Nat. Neurosci. 2013; 16: 357-364Crossref PubMed Scopus (126) Google Scholar, Varga et al., 2016Varga A.W. Ducca E.L. Kishi A. Fischer E. Parekh A. Koushyk V. Yau P.L. Gumb T. Leibert D.P. Wohlleber M.E. et al.Effects of aging on slow-wave sleep dynamics and human spatial navigational memory consolidation.Neurobiol. Aging. 2016; 42: 142-149Abstract Full Text Full Text PDF PubMed Google Scholar). Aβ further correlates with reduced REM sleep amount in healthy older adults (Mander et al., 2015Mander B.A. Marks S.M. Vogel J.W. Rao V. Lu B. Saletin J.M. Ancoli-Israel S. Jagust W.J. Walker M.P. β-amyloid disrupts human NREM slow waves and related hippocampus-dependent memory consolidation.Nat. Neurosci. 2015; 18: 1051-1057Crossref PubMed Scopus (75) Google Scholar) and patients with AD (Liguori et al., 2014Liguori C. Romigi A. Nuccetelli M. Zannino S. Sancesario G. Martorana A. Albanese M. Mercuri N.B. Izzi F. Bernardini S. et al.Orexinergic system dysregulation, sleep impairment, and cognitive decline in Alzheimer disease.JAMA Neurol. 2014; 71: 1498-1505Crossref PubMed Scopus (48) Google Scholar). This link may be connected to degeneration of REM-regulating cholinergic neurons projecting from the basal forebrain to the cortex (Brayet et al., 2015Brayet P. Petit D. Frauscher B. Gagnon J.F. Gosselin N. Gagnon K. Rouleau I. Montplaisir J. Quantitative EEG of rapid-eye-movement sleep: A marker of amnestic mild cognitive impairment.Clin. EEG Neurosci. 2015; 47: 134-141Crossref PubMed Scopus (2) Google Scholar, Gagnon et al., 2008Gagnon J.-F. Petit D. Latreille V. Montplaisir J. Neurobiology of sleep disturbances in neurodegenerative disorders.Curr. Pharm. Des. 2008; 14: 3430-3445Crossref PubMed Scopus (0) Google Scholar, Hassainia et al., 1997Hassainia F. Petit D. Nielsen T. Gauthier S. Montplaisir J. Quantitative EEG and statistical mapping of wakefulness and REM sleep in the evaluation of mild to moderate Alzheimer’s disease.Eur. Neurol. 1997; 37: 219-224Crossref PubMed Google Scholar, Moraes et al., 2006Moraes Wdos.S. Poyares D.R. Guilleminault C. Ramos L.R. Bertolucci P.H. Tufik S. The effect of donepezil on sleep and REM sleep EEG in patients with Alzheimer disease: a double-blind placebo-controlled study.Sleep. 2006; 29: 199-205Crossref PubMed Google Scholar, Petit et al., 2004Petit D. Gagnon J.F. Fantini M.L. Ferini-Strambi L. Montplaisir J. Sleep and quantitative EEG in neurodegenerative disorders.J. Psychosom. Res. 2004; 56: 487-496Abstract Full Text Full Text PDF PubMed Scopus (161) Google Scholar), though direct evidence remains lacking. In addition to Aβ, tau-associated neurofibrillary tangles within the medial temporal lobe are believed to represent an early stage in AD disease progression (Bouras et al., 1994Bouras C. Hof P.R. Giannakopoulos P. Michel J.P. Morrison J.H. Regional distribution of neurofibrillary tangles and senile plaques in the cerebral cortex of elderly patients: a quantitative evaluation of a one-year autopsy population from a geriatric hospital.Cereb. Cortex. 1994; 4: 138-150Crossref PubMed Google Scholar, Delacourte et al., 2002Delacourte A. Sergeant N. Wattez A. Maurage C.A. Lebert F. Pasquier F. David J.P. Tau aggregation in the hippocampal formation: an ageing or a pathological process?.Exp. Gerontol. 2002; 37: 1291-1296Crossref PubMed Scopus (59) Google Scholar, Jack et al., 2010Jack Jr., C.R. Knopman D.S. Jagust W.J. Shaw L.M. Aisen P.S. Weiner M.W. Petersen R.C. Trojanowski J.Q. Hypothetical model of dynamic biomarkers of the Alzheimer’s pathological cascade.Lancet Neurol. 2010; 9: 119-128Abstract Full Text Full Text PDF PubMed Scopus (1834) Google Scholar). Tau regional aggregation is relevant given the role of the hippocampus in generating ripples that are time locked to the expression of NREM sleep spindles and slow waves, hypothesized to support sleep-dependent declarative memory processing (Diekelmann and Born, 2010Diekelmann S. Born J. The memory function of sleep.Nat. Rev. Neurosci. 2010; 11: 114-126Crossref PubMed Scopus (13) Google Scholar, Staresina et al., 2015Staresina B.P. Bergmann T.O. Bonnefond M. van der Meij R. Jensen O. Deuker L. Elger C.E. Axmacher N. Fell J. Hierarchical nesting of slow oscillations, spindles and ripples in the human hippocampus during sleep.Nat. Neurosci. 2015; 18: 1679-1686Crossref PubMed Scopus (58) Google Scholar). Fitting this overlap, tau within the rodent brain is associated with disrupted NREM oscillations, leading to abnormally long (slow) hyperpolarized down state and a reduction in successful transitions to the depolarizing up state of the slow wave (Menkes-Caspi et al., 2015Menkes-Caspi N. Yamin H.G. Kellner V. Spires-Jones T.L. Cohen D. Stern E.A. Pathological tau disrupts ongoing network activity.Neuron. 2015; 85: 959-966Abstract Full Text Full Text PDF PubMed Google Scholar). In human studies, tau levels within cerebrospinal fluid are associated with diminished slow wave sleep in AD patients (Liguori et al., 2014Liguori C. Romigi A. Nuccetelli M. Zannino S. Sancesario G. Martorana A. Albanese M. Mercuri N.B. Izzi F. Bernardini S. et al.Orexinergic system dysregulation, sleep impairment, and cognitive decline in Alzheimer disease.JAMA Neurol. 2014; 71: 1498-1505Crossref PubMed Scopus (48) Google Scholar). Further supporting this tau-NREM oscillation hypothesis, both patients with mild cognitive impairment (MCI) and AD have significantly fewer posterior NREM fast sleep spindles relative to healthy older adults, with the degree of spindle reduction predicting the severity of memory impairment (Gorgoni et al., 2016Gorgoni M. Lauri G. Truglia I. Cordone S. Sarasso S. Scarpelli S. Mangiaruga A. D’Atri A. Tempesta D. Ferrara M. et al.Parietal fast sleep spindle density decrease in Alzheimer’s disease and amnesic mild cognitive impairment.Neural Plast. 2016; 2016: 8376108Crossref PubMed Scopus (2) Google Scholar, Rauchs et al., 2008Rauchs G. Schabus M. Parapatics S. Bertran F. Clochon P. Hot P. Denise P. Desgranges B. Eustache F. Gruber G. Anderer P. Is there a link between sleep changes and memory in Alzheimer’s disease?.Neuroreport. 2008; 19: 1159-1162Crossref PubMed Scopus (64) Google Scholar). However, studies are needed to verify which neuropathological factor explains this loss of posterior spindles and, if tau, whether this association is specific to AD or present in other tauopathies. Beyond the medial temporal lobe, AD post-mortem studies have established that neurofibrillary tangles within the preoptic area of the hypothalamus correlate with the severity of prior fragmented sleep (Lim et al., 2014Lim A.S. Ellison B.A. Wang J.L. Yu L. Schneider J.A. Buchman A.S. Bennett D.A. Saper C.B. Sleep is related to neuron numbers in the ventrolateral preoptic/intermediate nucleus in older adults with and without Alzheimer’s disease.Brain. 2014; 137: 2847-2861Crossref PubMed Scopus (0) Google Scholar). Interestingly, tau deposition is also present in other sleep-regulating areas such as the locus coeruleus and basal forebrain and can be observed even in cognitively normal older adults (Braak and Del Tredici, 2016Braak H. Del Tredici K. Potential pathways of abnormal tau and α-synuclein dissemination in sporadic Alzheimer’s and Parkinson’s diseases.Cold Spring Harb. Perspect. Biol. 2016; 8: 8Crossref Scopus (3) Google Scholar, Braak et al., 2011Braak H. Thal D.R. Ghebremedhin E. Del Tredici K. Stages of the pathologic process in Alzheimer disease: age categories from 1 to 100 years.J. Neuropathol. Exp. Neurol. 2011; 70: 960-969Crossref PubMed Scopus (401) Google Scholar, Stern and Naidoo, 2015Stern A.L. Naidoo N. Wake-active neurons across aging and neurodegeneration: a potential role for sleep disturbances in promoting disease.Springerplus. 2015; 4: 25Crossref PubMed Google Scholar). This leads to the currently untested hypothesis that tau within these regions may trigger sleep abnormalities years before degenerative disease onset and, if such sleep disruption is specific, could serve as an early diagnostic biomarker (Holth et al., 2016Holth J.K. Patel T.K. Holtzman D.M. Sleep in Alzheimer’s disease–beyond amyloid.Neurobiol. Sleep Circadian Rhythms. 2016; 2: 4-14Crossref PubMed Google Scholar). It is additionally becoming clear that the link between degenerative dementia conditions and sleep disruption is bi-directional. Work in mice has revealed an interacting mechanism, such that Aβ levels increase with time spent awake, while NREM sleep predicts the clearance of Aβ (Kang et al., 2009Kang J.E. Lim M.M. Bateman R.J. Lee J.J. Smyth L.P. Cirrito J.R. Fujiki N. Nishino S. Holtzman D.M. Amyloid-beta dynamics are regulated by orexin and the sleep-wake cycle.Science. 2009; 326: 1005-1007Crossref PubMed Scopus (420) Google Scholar, Xie et al., 2013Xie L. Kang H. Xu Q. Chen M.J. Liao Y. Thiyagarajan M. O’Donnell J. Christensen D.J. Nicholson C. Iliff J.J. et al.Sleep drives metabolite clearance from the adult brain.Science. 2013; 342: 373-377Crossref PubMed Scopus (718) Google Scholar). In cognitively normal older human adults, those with greater initial levels of sleep fragmentation go on to suffer a more rapid subsequent rate of cognitive decline and a higher risk of developing AD over an ensuing six-year period (Lim et al., 2013aLim A.S. Kowgier M. Yu L. Buchman A.S. Bennett D.A. Sleep fragmentation and the risk of incident Alzheimer’s disease and cognitive decline in older persons.Sleep. 2013; 36: 1027-1032Crossref PubMed Scopus (105) Google Scholar, Lim et al., 2013bLim A.S. Yu L. Kowgier M. Schneider J.A. Buchman A.S. Bennett D.A. Modification of the relationship of the apolipoprotein E ε4 allele to the risk of Alzheimer disease and neurofibrillary tangle density by sleep.JAMA Neurol. 2013; 70: 1544-1551Crossref PubMed Scopus (71) Google Scholar). These bi-directional relationships are observed before the onset of disease and, furthermore, independently of sleep disorders that also increase dementia risk, such as insomnia or sleep apnea (Osorio et al., 2011Osorio R.S. Pirraglia E. Agüera-Ortiz L.F. During E.H. Sacks H. Ayappa I. Walsleben J. Mooney A. Hussain A. Glodzik L. et al.Greater risk of Alzheimer’s disease in older adults with insomnia.J. Am. Geriatr. Soc. 2011; 59: 559-562Crossref PubMed Scopus (0) Google Scholar, Yaffe et al., 2011Yaffe K. Laffan A.M. Harrison S.L. Redline S. Spira A.P. Ensrud K.E. Ancoli-Israel S. Stone K.L. Sleep-disordered breathing, hypoxia, and risk of mild cognitive impairment and dementia in older women.JAMA. 2011; 306: 613-619Crossref PubMed Scopus (327) Google Scholar). It suggests that inadequate sleep is not only a predisposing risk factor contributing to degenerative disease processes, but represents a novel treatment opportunity and/or even preventative strategy in this context (Mander et al., 2016aMander B.A. Winer J.R. Jagust W.J. Walker M.P. Sleep: A novel mechanistic pathway, biomarker, and treatment target in the pathology of Alzheimer’s disease?.Trends Neurosci. 2016; 39: 552-566Abstract Full Text Full Text PDF PubMed Scopus (0) Google Scholar). In summary, dementia-related neuropathologies are associated with forms of sleep disruption that are uniquely distinct from typical age-related sleep disruption or, in some cases, a significantly more severe form of those same sleep impairments. The former is especially relevant in the context of sleep as a non-invasive and possible early biomarker distinguishing normal from abnormal aging. Beyond normative aging, sleep disruption is especially pervasive in neurodegenerative dementias. To date, the majority of pathological evidence concerns β-amyloid (Aβ) protein and tau neurofibrillary tangles that are characteristic of Alzheimer’s disease (AD). Subjective and objective measures of poor sleep correlate with cortical Aβ burden, as well as cerebrospinal fluid measures of Aβ and phosphorylated tau (Liguori et al., 2014Liguori C. Romigi A. Nuccetelli M. Zannino S. Sancesario G. Martorana A. Albanese M. Mercuri N.B. Izzi F. Bernardini S. et al.Orexinergic system dysregulation, sleep impairment, and cognitive decline in Alzheimer disease.JAMA Neurol. 2014; 71: 1498-1505Crossref PubMed Scopus (48) Google Scholar, Mander et al., 2015Mander B.A. Marks S.M. Vogel J.W. Rao V. Lu B. Saletin J.M. Ancoli-Israel S. Jagust W.J. Walker M.P. β-amyloid disrupts human NREM slow waves and related hippocampus-dependent memory consolidation.Nat. Neurosci. 2015; 18: 1051-1057Crossref PubMed Scopus (75) Google Scholar, Spira et al., 2013Spira A.P. Gamaldo A.A. An Y. Wu M.N. Simonsick E.M. Bilgel M. Zhou Y. Wong D.F. Ferrucci L. Resnick S.M. Self-reported sleep and β-amyloid deposition in community-dwelling older adults.JAMA Neurol. 2013; 70: 1537-1543Crossref PubMed Scopus (114) Google Scholar, Sprecher et al., 2015Sprecher K.E. Bendlin B.B. Racine A.M. Okonkwo O.C. Christian B.T. Koscik R.L. Sager M.A. Asthana S. Johnson S.C. Benca R.M. Amyloid burden is associated with self-reported sleep in nondemented late middle-aged adults.Neurobiol. Aging. 2015; 36: 2568-2576Abstract Full Text Full Text PDF PubMed Scopus (32) Google Scholar). Similar associations have been observed in animals, with Aβ accumulation in rodent models of AD predicting greater sleep fragmentation (Roh et al., 2012Roh J.H. Huang Y. Bero A.W. Kasten T. Stewart F.R. Bateman R.J. Holtzman D.M. Disruption of the sleep-wake cycle and diurnal fluctuation of β-amyloid in mice with Alzheimer’s disease pathology.Sci. Transl. Med. 2012; 4: 150ra122Crossref PubMed Scopus (133) Google Scholar). Recent studies in humans have further established that Aβ is selectively associated with the loss of <1 Hz NREM sleep oscillations (Mander et al., 2015Mander B.A. Marks S.M. Vogel J.W. Rao V. Lu B. Saletin J.M. Ancoli-Israel S. Jagust W.J. Walker M.P. β-amyloid disrupts human NREM slow waves and related hippocampus-dependent memory consolidation.Nat. Neurosci. 2015; 18: 1051-1057Crossref PubMed Scopus (75) Google Scholar). This association between Aβ and <1 Hz NREM oscillations appears to be unique and distinct from general age-related reductions in the broader SWA range of 0.6–4.8 Hz; with the latter linked, instead, to gray matter atrophy within the medial prefrontal cortex (Dubé et al., 2015Dubé J. Lafortune M. Bedetti C. Bouchard M. Gagnon J.F. Doyon J. Evans A.C. Lina J.M. Carrier J. Cortical thinning explains changes in sleep slow waves during adulthood.J. Neurosci. 2015; 35: 7795-7807Crossref PubMed Scopus (5) Google Scholar, Mander et al., 2013Mander B.A. Rao V. Lu B. Saletin J.M. Lindquist J.R. Ancoli-Israel S. Jagust W. Walker M.P. Prefrontal atrophy, disrupted NREM slow waves and impaired hippocampal-dependent memory in aging.Nat. Neurosci. 2013; 16: 357-364Crossref PubMed Scopus (126) Google Scholar, Varga et al., 2016Varga A.W. Ducca E.L. Kishi A. Fischer E. Parekh A. Koushyk V. Yau P.L. Gumb T. Leibert D.P. Wohlleber M.E. et al.Effects of aging on slow-wave sleep dynamics and human spatial navigational memory consolidation.Neurobiol. Aging. 2016; 42: 142-149Abstract Full Text Full Text PDF PubMed Google Scholar). Aβ further correlates with reduced REM sleep amount in healthy older adults (Mander et al., 2015Mander B.A. Marks S.M. Vogel J.W. Rao V. Lu B. Saletin J.M. Ancoli-Israel S. Jagust W.J. Walker M.P. β-amyloid disrupts human NREM slow waves and related hippocampus-dependent memory consolidation.Nat. Neurosci. 2015; 18: 1051-1057Crossref PubMed Scopus (75) Google Scholar) and patients with AD (Liguori et al., 2014Liguori C. Romigi A. Nuccetelli M. Zannino S. Sancesario G. Martorana A. Albanese M. Mercuri N.B. Izzi F. Bernardini S. et al.Orexinergic system dysregulation, sleep impairment, and cognitive decline in Alzheimer disease.JAMA Neurol. 2014; 71: 1498-1505Crossref PubMed Scopus (48) Google Scholar). This link may be connected to degeneration of REM-regulating cholinergic neurons projecting from the basal forebrain to the cortex (Brayet et al., 2015Brayet P. Petit D. Frauscher B. Gagnon J.F. Gosselin N. Gagnon K. Rouleau I. Montplaisir J. Quantitative EEG of rapid-eye-movement sleep: A marker of amnestic mild cognitive impairment.Clin. EEG Neurosci. 2015; 47: 134-141Crossref PubMed Scopus (2) Google Scholar, Gagnon et al., 2008Gagnon J.-F. Petit D. Latreille V. Montplaisir J. Neurobiology of sleep disturbances in neurodegenerative disorders.Curr. Pharm. Des. 2008; 14: 3430-3445Crossref PubMed Scopus (0) Google Scholar, Hassainia et al., 1997Hassainia F. Petit D. Nielsen T. Gauthier S. Montplaisir J. Quantitative EEG and statistical mapping of wakefulness and REM sleep in the evaluation of mild to moderate Alzheimer’s disease.Eur. Neurol. 1997; 37: 219-224Crossref PubMed Google Scholar, Moraes et al., 2006Moraes Wdos.S. Poyares D.R. Guilleminault C. Ramos L.R. Bertolucci P.H. Tufik S. The effect of donepezil on sleep and REM sleep EEG in patients with Alzheimer disease: a double-blind placebo-controlled study.Sleep. 2006; 29: 199-205Crossref PubMed Google Scholar, Petit et al., 2004Petit D. Gagnon J.F. Fantini M.L. Ferini-Strambi L. Montplaisir J. Sleep and quantitative EEG in neurodegenerative disorders.J. Psychosom. Res. 2004; 56: 487-496Abstract Full Text Full Text PDF PubMed Scopus (161) Google Scholar), though direct evidence remains lacking. In addition to Aβ, tau-associated neurofibrillary tangles within the medial temporal lobe are believed to represent an early stage in AD disease progression (Bouras et al., 1994Bouras C. Hof P.R. Giannakopoulos P. Michel J.P. Morrison J.H. Regional distribution of neurofibrillary tangles and senile plaques in the cerebral cortex of elderly patients: a quantitative evaluation of a one-year autopsy population from a geriatric hospital.Cereb. Cortex. 1994; 4: 138-150Crossref PubMed Google Scholar, Delacourte et al., 2002Delacourte A. Sergeant N. Wattez A. Maurage C.A. Lebert F. Pasquier F. David J.P. Tau aggregation in the hippocampal formation: an ageing or a pathological process?.Exp. Gerontol. 2002; 37: 1291-1296Crossref PubMed Scopus (59) Google Scholar, Jack et al., 2010Jack Jr., C.R. Knopman D.S. Jagust W.J. Shaw L.M. Aisen P.S. Weiner M.W. Petersen R.C. Trojanowski J.Q. Hypothetical model of dynamic biomarkers of the Alzheimer’s pathological cascade.Lancet Neurol. 20" @default.
• W2605277320 created "2017-04-14" @default.
• W2605277320 creator A5022724258 @default.
• W2605277320 creator A5074458586 @default.
• W2605277320 creator A5074973044 @default.
• W2605277320 date "2017-04-01" @default.
• W2605277320 modified "2023-10-14" @default.
• W2605277320 title "Sleep and Human Aging" @default.
• W2605277320 cites W1016472498 @default.
• W2605277320 cites W1500835114 @default.
• W2605277320 cites W1507624770 @default.
• W2605277320 cites W1510126674 @default.
• W2605277320 cites W1513102925 @default.
• W2605277320 cites W1545353838 @default.
• W2605277320 cites W1573371752 @default.
• W2605277320 cites W1576210090 @default.
• W2605277320 cites W1590813564 @default.
• W2605277320 cites W1720853336 @default.
• W2605277320 cites W1844614575 @default.
• W2605277320 cites W1917877419 @default.
• W2605277320 cites W1930930875 @default.
• W2605277320 cites W1960756182 @default.
• W2605277320 cites W1964122385 @default.
• W2605277320 cites W1966657660 @default.
• W2605277320 cites W1966770839 @default.
• W2605277320 cites W1968693054 @default.
• W2605277320 cites W1969535988 @default.
• W2605277320 cites W1971730406 @default.
• W2605277320 cites W1972234961 @default.
• W2605277320 cites W1973882489 @default.
• W2605277320 cites W1975136983 @default.
• W2605277320 cites W1983620103 @default.
• W2605277320 cites W1990071063 @default.
• W2605277320 cites W1991104142 @default.
• W2605277320 cites W1991934169 @default.
• W2605277320 cites W1993023011 @default.
• W2605277320 cites W1998684886 @default.
• W2605277320 cites W1999783755 @default.
• W2605277320 cites W2000195699 @default.
• W2605277320 cites W2002378420 @default.
• W2605277320 cites W2007283165 @default.
• W2605277320 cites W2007642463 @default.
• W2605277320 cites W2011580879 @default.
• W2605277320 cites W2012446274 @default.
• W2605277320 cites W2012783828 @default.
• W2605277320 cites W2013006955 @default.
• W2605277320 cites W2013333500 @default.
• W2605277320 cites W2013563458 @default.
• W2605277320 cites W2015603515 @default.
• W2605277320 cites W2015970163 @default.
• W2605277320 cites W2018354461 @default.
• W2605277320 cites W2018788799 @default.
• W2605277320 cites W2019174868 @default.
• W2605277320 cites W2020676537 @default.
• W2605277320 cites W2023689431 @default.
• W2605277320 cites W2026434433 @default.
• W2605277320 cites W2027637480 @default.
• W2605277320 cites W2028899342 @default.
• W2605277320 cites W2029151785 @default.
• W2605277320 cites W2030353060 @default.
• W2605277320 cites W2032683219 @default.
• W2605277320 cites W2034489750 @default.
• W2605277320 cites W2035490031 @default.
• W2605277320 cites W2036187063 @default.
• W2605277320 cites W2037268341 @default.
• W2605277320 cites W2037573884 @default.
• W2605277320 cites W2038309664 @default.
• W2605277320 cites W2038599263 @default.
• W2605277320 cites W2040853845 @default.
• W2605277320 cites W2041098567 @default.
• W2605277320 cites W2042680190 @default.
• W2605277320 cites W2043181113 @default.
• W2605277320 cites W2043909860 @default.
• W2605277320 cites W2044084156 @default.
• W2605277320 cites W2044652084 @default.
• W2605277320 cites W2045815714 @default.
• W2605277320 cites W2054305273 @default.
• W2605277320 cites W2055916672 @default.
• W2605277320 cites W2056787679 @default.
• W2605277320 cites W2058811410 @default.
• W2605277320 cites W2059110708 @default.
• W2605277320 cites W2060964963 @default.
• W2605277320 cites W2071039532 @default.
• W2605277320 cites W2073025039 @default.
• W2605277320 cites W2076136875 @default.
• W2605277320 cites W2076327464 @default.
• W2605277320 cites W2076985735 @default.
• W2605277320 cites W2082429191 @default.
• W2605277320 cites W2082883998 @default.
• W2605277320 cites W2083352270 @default.
• W2605277320 cites W2084108448 @default.
• W2605277320 cites W2084595451 @default.
• W2605277320 cites W2084617650 @default.
• W2605277320 cites W2085186337 @default.
• W2605277320 cites W2085977004 @default.
• W2605277320 cites W2089225551 @default.
• W2605277320 cites W2089424110 @default.
• W2605277320 cites W2090240067 @default.

• next