Xiaowen Zhou, Guangshi Zhang, Qili Hu, Hanyu Shao, Tao Yang, Jie Wang, Xiaoniu Liang, Qianhua Zhao, Ding Ding
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引用次数: 0
Abstract
Introduction: Excessive daytime sleepiness (EDS) is common in community-dwelling older adults, but its association with long-term incident dementia remains unclear. The roles of Alzheimer's disease (AD) pathology and vascular-related white matter injury in this association were merely studied.
Methods: We included 617 dementia-free participants from the Shanghai Aging Study with up to 10 years of follow-up. At baseline, EDS was assessed with the Epworth Sleepiness Scale (ESS) and plasma phosphorylated tau (p-tau)217 was measured using a single-molecule immune-array assay. Cognitive decline was evaluated using the Mini-Mental State Examination (MMSE), and incident dementia was determined by expert consensus during follow-up. A magnetic resonance imaging marker of white matter injury (peak width of skeletonized mean diffusivity [PSMD]) was derived from diffusion tensor imaging, and gray matter volume was assessed from T1-weighted imaging in a subcohort.
Results: At baseline, 66 participants (10.7%) had EDS and showed lower MMSE scores. EDS was associated with a higher risk of incident dementia (hazard ratio [HR] 2.06, 95% confidence interval [CI] 1.09-3.92), especially among individuals with low p-tau217 (HR 4.94, 95% CI 1.75-13.93) independent of sleep disturbance after adjusting for age, sex, and education. Higher ESS was related to AD pathology-dependent patterns of brain atrophy and to higher PSMD. PSMD modified the associations between EDS and cognitive decline, and incident dementia. Participants with both high PSMD and EDS showed the highest dementia risk.
Discussion: EDS may help identify older adults with low AD biomarker burden who are at increased risk of dementia, independent of nocturnal sleep disturbance. White matter injury may contribute to this risk, supporting a vascular vulnerability pathway.
期刊介绍:
Alzheimer''s & Dementia: Translational Research & Clinical Interventions (TRCI) is a peer-reviewed, open access,journal from the Alzheimer''s Association®. The journal seeks to bridge the full scope of explorations between basic research on drug discovery and clinical studies, validating putative therapies for aging-related chronic brain conditions that affect cognition, motor functions, and other behavioral or clinical symptoms associated with all forms dementia and Alzheimer''s disease. The journal will publish findings from diverse domains of research and disciplines to accelerate the conversion of abstract facts into practical knowledge: specifically, to translate what is learned at the bench into bedside applications. The journal seeks to publish articles that go beyond a singular emphasis on either basic drug discovery research or clinical research. Rather, an important theme of articles will be the linkages between and among the various discrete steps in the complex continuum of therapy development. For rapid communication among a multidisciplinary research audience involving the range of therapeutic interventions, TRCI will consider only original contributions that include feature length research articles, systematic reviews, meta-analyses, brief reports, narrative reviews, commentaries, letters, perspectives, and research news that would advance wide range of interventions to ameliorate symptoms or alter the progression of chronic neurocognitive disorders such as dementia and Alzheimer''s disease. The journal will publish on topics related to medicine, geriatrics, neuroscience, neurophysiology, neurology, psychiatry, clinical psychology, bioinformatics, pharmaco-genetics, regulatory issues, health economics, pharmacoeconomics, and public health policy as these apply to preclinical and clinical research on therapeutics.