Sleep Quality and Preclinical Alzheimer Disease

被引:512
作者
Ju, Yo-El S. [1 ]
McLeland, Jennifer S. [1 ]
Toedebusch, Cristina D. [1 ]
Xiong, Chengjie [2 ,3 ]
Fagan, Anne M. [1 ,2 ,4 ]
Duntley, Stephen P. [1 ]
Morris, John C. [1 ,2 ]
Holtzman, David M. [1 ,2 ,4 ]
机构
[1] Washington Univ, Sch Med, Dept Neurol, St Louis, MO 63110 USA
[2] Washington Univ, Sch Med, Charles F & Joanne Knight Alzheimers Dis Res Ctr, St Louis, MO 63110 USA
[3] Washington Univ, Sch Med, Div Biostat, St Louis, MO 63110 USA
[4] Washington Univ, Sch Med, Hope Ctr Neurol Disorders, St Louis, MO 63110 USA
基金
美国国家卫生研究院;
关键词
MILD COGNITIVE IMPAIRMENT; OLDER WOMEN; AMYLOID DEPOSITION; BETA DYNAMICS; IN-VIVO; A-BETA; DEMENTIA; DECLINE; DISTURBANCE; DURATION;
D O I
10.1001/jamaneurol.2013.2334
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Importance: Sleep and circadian problems are very common in Alzheimer disease (AD). Recent animal studies suggest a bidirectional relationship between sleep and beta-amyloid (A beta), a key molecule involved in AD pathogenesis. Objective: To test whether A beta deposition in preclinical AD, prior to the appearance of cognitive impairment, is associated with changes in quality or quantity of sleep. Design: Cross-sectional study conducted from October 2010 to June 2012. Setting: General community volunteers at the Washington University Knight Alzheimer's Disease Research Center. Participants: Cognitively normal individuals (n=145) 45 years and older were recruited from longitudinal studies of memory and aging at the Washington University Knight Alzheimer's Disease Research Center. Valid actigraphy data were recorded in 142. The majority (124 of 142) were recruited from the Adult Children Study, in which all were aged 45 to 75 years at baseline and 50% have a parental history of late-onset AD. The rest were recruited from a community volunteer cohort in which all were older than 60 years and healthy at baseline. Main Outcome Measures: Sleep was objectively measured using actigraphy for 2 weeks. Sleep efficiency, which is the percentage of time in bed spent asleep, was the primary measure of sleep quality. Total sleep time was the primary measure of sleep quantity. Cerebrospinal fluid A beta 42 levels were used to determine whether amyloid deposition was present or absent. Concurrent sleep diaries provided nap information. Results: Amyloid deposition, as assessed by A beta 42 levels, was present in 32 participants (22.5%). This group had worse sleep quality, as measured by sleep efficiency (80.4% vs 83.7%), compared with those without amyloid deposition, after correction for age, sex, and APOE epsilon 4 allele carrier status (P=.04). In contrast, quantity of sleep was not significantly different between groups, as measured by total sleep time. Frequent napping, 3 or more days per week, was associated with amyloid deposition (31.2% vs 14.7%; P=.03). Conclusions and Relevance: Amyloid deposition in the preclinical stage of AD appears to be associated with worse sleep quality but not with changes in sleep quantity.
引用
收藏
页码:587 / 593
页数:7
相关论文
共 39 条
[1]  
AncoliIsrael S, 1997, SLEEP, V20, P18
[2]   DEMENTIA IN INSTITUTIONALIZED ELDERLY - RELATION TO SLEEP-APNEA [J].
ANCOLIISRAEL, S ;
KLAUBER, MR ;
BUTTERS, N ;
PARKER, L ;
KRIPKE, DF .
JOURNAL OF THE AMERICAN GERIATRICS SOCIETY, 1991, 39 (03) :258-263
[3]   Clinical and Biomarker Changes in Dominantly Inherited Alzheimer's Disease [J].
Bateman, Randall J. ;
Xiong, Chengjie ;
Benzinger, Tammie L. S. ;
Fagan, Anne M. ;
Goate, Alison ;
Fox, Nick C. ;
Marcus, Daniel S. ;
Cairns, Nigel J. ;
Xie, Xianyun ;
Blazey, Tyler M. ;
Holtzman, David M. ;
Santacruz, Anna ;
Buckles, Virginia ;
Oliver, Angela ;
Moulder, Krista ;
Aisen, Paul S. ;
Ghetti, Bernardino ;
Klunk, William E. ;
McDade, Eric ;
Martins, Ralph N. ;
Masters, Colin L. ;
Mayeux, Richard ;
Ringman, John M. ;
Rossor, Martin N. ;
Schofield, Peter R. ;
Sperling, Reisa A. ;
Salloway, Stephen ;
Morris, John C. .
NEW ENGLAND JOURNAL OF MEDICINE, 2012, 367 (09) :795-804
[4]   Neuronal activity regulates the regional vulnerability to amyloid-β deposition [J].
Bero, Adam W. ;
Yan, Ping ;
Roh, Jee Hoon ;
Cirrito, John R. ;
Stewart, Floy R. ;
Raichle, Marcus E. ;
Lee, Jin-Moo ;
Holtzman, David M. .
NATURE NEUROSCIENCE, 2011, 14 (06) :750-U353
[5]   Poor sleep is associated with impaired cognitive function in older women: The Study of Osteoporotic Fractures [J].
Blackwell, T ;
Yaffe, K ;
Ancoli-Israel, S ;
Scheider, JL ;
Cauley, JA ;
Hillier, TA ;
Fink, HA ;
Stone, KL .
JOURNALS OF GERONTOLOGY SERIES A-BIOLOGICAL SCIENCES AND MEDICAL SCIENCES, 2006, 61 (04) :405-410
[6]   NEUROPATHOLOGICAL STAGING OF ALZHEIMER-RELATED CHANGES [J].
BRAAK, H ;
BRAAK, E .
ACTA NEUROPATHOLOGICA, 1991, 82 (04) :239-259
[7]   Synaptic activity regulates interstitial fluid amyloid-β levels in vivo [J].
Cirrito, JR ;
Yamada, KA ;
Finn, MB ;
Sloviter, RS ;
Bales, KR ;
May, PC ;
Schoepp, DD ;
Paul, SM ;
Mennerick, S ;
Holtzman, DM .
NEURON, 2005, 48 (06) :913-922
[8]   Inverse relation between in vivo amyloid imaging load and cerebrospinal fluid Aβ42 in humans [J].
Fagan, AM ;
Mintun, MA ;
Mach, RH ;
Lee, SY ;
Dence, CS ;
Shah, AR ;
LaRossa, GN ;
Spinner, ML ;
Klunk, WE ;
Mathis, CA ;
DeKosky, ST ;
Morris, JC ;
Holtzman, DM .
ANNALS OF NEUROLOGY, 2006, 59 (03) :512-519
[9]   Cerebrospinal fluid tau/β-amyloid42 ratio as a prediction of cognitive decline in nondemented older adults [J].
Fagan, Anne M. ;
Roe, Catherine M. ;
Xiong, Chengjie ;
Mintun, Mark A. ;
Morris, John C. ;
Holtzman, David M. .
ARCHIVES OF NEUROLOGY, 2007, 64 (03) :343-349
[10]   Cerebrospinal fluid tau and ptau181 increase with cortical amyloid deposition in cognitively normal individuals: Implications for future clinical trials of Alzheimer's disease [J].
Fagan, Anne M. ;
Mintun, Mark A. ;
Shah, Aarti R. ;
Aldea, Patricia ;
Roe, Catherine M. ;
Mach, Robert H. ;
Marcus, Daniel ;
Morris, John C. ;
Holtzman, David M. .
EMBO MOLECULAR MEDICINE, 2009, 1 (8-9) :371-380