期刊
JOURNAL OF ALZHEIMERS DISEASE
卷 81, 期 4, 页码 1701-1710出版社
IOS PRESS
DOI: 10.3233/JAD-201582
关键词
Amyloid-beta; cognition; insomnia; interaction; longitudinal
资金
- National Natural Science Foundation of China [82001136, 81901121]
- Alzheimer's Disease Neuroimaging Initiative (ADNI) (National Institutes of Health) [U01 AG024904]
- DOD ADNI (Department of Defense) [W81XWH-12-2-0012]
- National Institute on Aging
- National Institute of Biomedical Imaging and Bioengineering
- AbbVie
- Alzheimer's Association
- Alzheimer's Drug Discovery Foundation
- Araclon Biotech
- BioClinica, Inc.
- Biogen
- Bristol-Myers Squibb Company
- CereSpir, Inc.
- Cogstate
- Eisai Inc.
- Elan Pharmaceuticals, Inc.
- Eli Lilly and Company
- EuroImmun
- F. Hoffmann-La Roche Ltd and its affiliated company Genentech, Inc.
- Fujirebio
- GE Healthcare
- IXICO Ltd.
- Janssen Alzheimer Immunotherapy Research & Development, LLC.
- Johnson & Johnson Pharmaceutical Research & Development LLC.
- Lumosity
- Lundbeck
- Merck Co., Inc.
- Meso Scale Diagnostics, LLC.
- NeuroRx Research
- Neurotrack Technologies
- Novartis Pharmaceuticals Corporation
- Pfizer Inc.
- Piramal Imaging
- Servier
- Takeda Pharmaceutical Company
- Transition Therapeutics
- Canadian Institutes of Health Research
Insomnia may modulate the relationship between amyloid-beta and cognitive performance in older adults, with individuals having elevated A beta and insomnia experiencing faster cognitive decline.
Background: It is suggested that not all individuals with elevated A beta will develop dementia or cognitive impairment. Environment or lifestyle might modulate the association of amyloid pathology with cognition. Insomnia is a risk factor of cognitive disorders including Alzheimer's disease. Objective: To investigate if insomnia moderated the relationship between amyloid-beta (A beta) and longitudinal cognitive performance in non-demented elders. Methods: A total of 385 Alzheimer's Disease Neuroimaging Initiative participants (mean age = 73 years, 48% females) who completed 4 + neuropsychological evaluations and a [F-18] florbetapir positron emission tomography scan were followed up to 8 years. Linear mixed-effects regression models were used to examine the interactions effect between insomnia and A beta on longitudinal cognitive sores, including four domains (memory [MEM], executive function [EF], language [LAN], and visuospatial function [VS]). Results: The A beta-positive status (A+) but not insomnia independently predicted faster cognitive decline in all domains. Furthermore, the relationship between A beta and cognitive decline was moderated by insomnia (MEM: chi(2) = 4.05, p = 0.044, EF: chi(2) = 4.38, p = 0.036, LAN: chi(2) = 4.56, p = 0.033, and VS: chi(2) = 4.12, p = 0.042). Individuals with both elevated A beta and insomnia experienced faster cognitive decline than those with only elevated A beta or insomnia. Conclusion: These data reinforced the values of insomnia management in preventing dementia, possibly by interacting A beta metabolism. Future efforts are warranted to determine whether sleep improvement will postpone the onset of dementia, specifically among populations in stages of preclinical or prodromal AD.
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