Dysfunction of circadian and sleep rhythms in the early stages of Alzheimer's disease

被引:25
作者
Rigat, Ludovica [1 ,2 ]
Ouk, Koliane [1 ,2 ]
Kramer, Achim [3 ]
Priller, Josef [1 ,2 ,4 ,5 ,6 ,7 ,8 ]
机构
[1] Charite Univ Med Berlin, Neuropsychiat, Charitepl 1, D-10117 Berlin, Germany
[2] Charite Univ Med Berlin, Lab Mol Psychiat, Charitepl 1, D-10117 Berlin, Germany
[3] Charite Univ Med Berlin, Div Chronobiol, Charitepl 1, D-10117 Berlin, Germany
[4] German Ctr Neurodegenerat Dis DZNE, D-10117 Berlin, Germany
[5] Tech Univ Munich, Sch Med & Hlth, Dept Psychiat & Psychotherapy, Ismaninger Str 22, D-81675 Munich, Germany
[6] UK Dementia Res Inst, Ctr Clin Brain Sci, 49 Little France Crescent, Edinburgh EH16 4SB, Scotland
[7] Charite Univ Med Berlin, Neuropsychiat, Charitepl 1, D-10117 Berlin, Germany
[8] Charite Univ Med Berlin, Lab Mol Psychiat, Charitepl 1, D-10117 Berlin, Germany
关键词
Alzheimer's disease; circadian system; clock; neurodegeneration; sleep; LIGHT THERAPY; COGNITIVE IMPAIRMENT; CLOCK PROTEINS; BRIGHT-LIGHT; SHIFT WORK; REV-ERB; MELATONIN; DEMENTIA; TIME; CRYPTOCHROME;
D O I
10.1111/apha.13970
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
Dysfunction of circadian and sleep rhythms is an early feature of many neurodegenerative diseases. Alzheimer's disease (AD) is a progressive neurodegenerative disorder resulting in cognitive and psychiatric disturbances. Although it is largely unclear whether dysfunctions in sleep and circadian rhythms contribute to the etiology of AD or are a consequence of the disease, there is evidence that these conditions are involved in a complex self-reinforcing bidirectional relationship. According to the recent studies, dysregulation of the circadian clock already occurs during the asymptomatic stage of the disease and could promote neurodegeneration. Thus, restoration of sleep and circadian rhythms in preclinical AD may represent an opportunity for early intervention to slow the disease course.
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页数:13
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共 126 条
[41]  
Homolak Jan, 2018, Med Sci (Basel), V6, DOI [10.3390/medsci6030052, 10.3390/medsci6030052]
[42]   Circadian clocks, cognition, and Alzheimer's disease: synaptic mechanisms, signaling effectors, and chronotherapeutics [J].
Hoyt, Kari R. ;
Obrietan, Karl .
MOLECULAR NEURODEGENERATION, 2022, 17 (01)
[43]   The circadian clock regulates autophagy directly through the nuclear hormone receptor Nr1d1/Rev-erb and indirectly via Cebpb/(C/ebp) in zebrafish [J].
Huang, Guodong ;
Zhang, Fanmiao ;
Ye, Qiang ;
Wang, Han .
AUTOPHAGY, 2016, 12 (08) :1292-1309
[44]   Photic Regulation of Clock Systems [J].
Hughes, Steven ;
Jagannath, Aarti ;
Hankins, Mark W. ;
Foster, Russell G. ;
Peirson, Stuart N. .
CIRCADIAN RHYTHMS AND BIOLOGICAL CLOCKS, PT B, 2015, 552 :125-143
[45]   Epigenetic Regulation of BMAL1 with Sleep Disturbances and Alzheimer's Disease [J].
Hulme, Bethany ;
Didikoglu, Altug ;
Bradburn, Steven ;
Robinson, Andrew ;
Canal, Maria ;
Payton, Antony ;
Pendleton, Neil ;
Murgatroyd, Chris .
JOURNAL OF ALZHEIMERS DISEASE, 2020, 77 (04) :1783-1792
[46]   Association of Sleep and β-Amyloid Pathology Among Older Cognitively Unimpaired Adults [J].
Insel, Philip S. ;
Mohlenhoff, Brian S. ;
Neylan, Thomas C. ;
Krystal, Andrew D. ;
Mackin, R. Scott .
JAMA NETWORK OPEN, 2021, 4 (07)
[47]   Prevalence of Cerebral Amyloid Pathology in Persons Without Dementia A Meta-analysis [J].
Jansen, Willemijn J. ;
Ossenkoppele, Rik ;
Knol, Dirk L. ;
Tijms, Betty M. ;
Scheltens, Philip ;
Verhey, Frans R. J. ;
Visser, Pieter Jelle .
JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION, 2015, 313 (19) :1924-1938
[48]   The incidence of dementia - A meta-analysis [J].
Jorm, AF ;
Jolley, D .
NEUROLOGY, 1998, 51 (03) :728-733
[49]   Sleep and Alzheimer disease pathology-a bidirectional relationship [J].
Ju, Yo-El S. ;
Lucey, Brendan P. ;
Holtzman, David M. .
NATURE REVIEWS NEUROLOGY, 2014, 10 (02) :115-119
[50]   Sleep Quality and Preclinical Alzheimer Disease [J].
Ju, Yo-El S. ;
McLeland, Jennifer S. ;
Toedebusch, Cristina D. ;
Xiong, Chengjie ;
Fagan, Anne M. ;
Duntley, Stephen P. ;
Morris, John C. ;
Holtzman, David M. .
JAMA NEUROLOGY, 2013, 70 (05) :587-593