Association of Excessive Daytime Sleepiness With Long-Term Incident Dementia: The Role of β-Amyloid and White Matter Injury.

IF 7.4 Q1 CLINICAL NEUROLOGY
Xiaowen Zhou, Guangshi Zhang, Qili Hu, Hanyu Shao, Tao Yang, Jie Wang, Xiaoniu Liang, Qianhua Zhao, Ding Ding
{"title":"Association of Excessive Daytime Sleepiness With Long-Term Incident Dementia: The Role of β-Amyloid and White Matter Injury.","authors":"Xiaowen Zhou, Guangshi Zhang, Qili Hu, Hanyu Shao, Tao Yang, Jie Wang, Xiaoniu Liang, Qianhua Zhao, Ding Ding","doi":"10.1002/trc2.70272","DOIUrl":null,"url":null,"abstract":"<p><strong>Introduction: </strong>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.</p><p><strong>Methods: </strong>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.</p><p><strong>Results: </strong>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.</p><p><strong>Discussion: </strong>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.</p>","PeriodicalId":53225,"journal":{"name":"Alzheimer''s and Dementia: Translational Research and Clinical Interventions","volume":"12 2","pages":"e70272"},"PeriodicalIF":7.4000,"publicationDate":"2026-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13239897/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Alzheimer''s and Dementia: Translational Research and Clinical Interventions","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1002/trc2.70272","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2026/4/1 0:00:00","PubModel":"eCollection","JCR":"Q1","JCRName":"CLINICAL NEUROLOGY","Score":null,"Total":0}
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.

日间过度嗜睡与长期痴呆的关系:β-淀粉样蛋白和白质损伤的作用。
日间过度嗜睡(EDS)在社区居住的老年人中很常见,但其与长期痴呆的关系尚不清楚。阿尔茨海默病(AD)病理和血管相关白质损伤在这一关联中的作用仅被研究。方法:我们从上海老龄化研究中纳入了617名无痴呆的参与者,随访时间长达10年。基线时,使用Epworth嗜睡量表(ESS)评估EDS,使用单分子免疫阵列测定血浆磷酸化tau蛋白(p-tau)217。使用简易精神状态检查(MMSE)评估认知能力下降,并在随访期间通过专家共识确定痴呆发生率。通过扩散张量成像得出白质损伤的磁共振成像标记物(骨化平均扩散率峰宽[PSMD]),并通过亚队列中的t1加权成像评估灰质体积。结果:在基线时,66名参与者(10.7%)患有EDS, MMSE评分较低。EDS与较高的痴呆发生率相关(风险比[HR] 2.06, 95%可信区间[CI] 1.09-3.92),特别是在调整年龄、性别和教育程度后,独立于睡眠障碍的p-tau217低(HR 4.94, 95% CI 1.75-13.93)的个体中。高ESS与AD病理依赖的脑萎缩模式和高PSMD有关。PSMD改变了EDS与认知能力下降和痴呆发生率之间的关系。同时患有PSMD和EDS的参与者患痴呆的风险最高。讨论:EDS可能有助于识别老年痴呆症风险增加的AD生物标志物负担低的老年人,独立于夜间睡眠障碍。白质损伤可能导致这种风险,支持血管易损途径。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
CiteScore
10.10
自引率
2.10%
发文量
134
审稿时长
10 weeks
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.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:604180095
Book学术官方微信
小红书