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Rationale and design of a multidomain lifestyle program for mild cognitive impairment 轻度认知障碍的多领域生活方式方案的基本原理和设计
IF 11.1 1区 医学 Q1 CLINICAL NEUROLOGY
Alzheimer's & Dementia
Pub Date : 2026-01-28 DOI: 10.1002/alz.71068
Amy D. Rodriguez, Jennifer R. DuBose, Agata Rozga, Craig M. Zimring, Elizabeth D. Mynatt, Gari D. Clifford, Kayci L. Vickers, Felicia C. Goldstein, Emily L. Giannotto, Jacquelyn Thelin, Allan I. Levey

The development of non-pharmacological treatment approaches is supported by evidence that addressing key modifiable risk factors may prevent or delay up to 45% of dementia cases. The Charlie and Harriet Shaffer Cognitive Empowerment Program (CEP) was developed to address current gaps in access to, and evidence for, interventions that reduce lifestyle risk factors and improve quality of life in individuals with mild cognitive impairment (MCI). Co-designed with patients and families, clinicians, researchers, and industry professionals, the CEP is situated in a conceptual framework that guides assessments and interventions/supports to holistically address the experience of living with MCI. CEP comprises four cores (Therapeutic Programs, Technology, Built Environment, and Innovation Accelerator) that map to the conceptual framework. We contend that our approach provides an opportunity to contribute to the evidence base for multidomain lifestyle programs and gain a deeper understanding of MCI and how individuals can be empowered to manage it.

Highlights

  • The cognitive empowerment program (CEP) is a multidomain lifestyle program that was developed using a co-design process and a conceptual framework that holistically addresses the experience of living with mild cognitive impairment (MCI).
  • CEP provides comprehensive assessment and intervention/support through four cores that map to the conceptual framework: therapeutic programs, technology, built environment and research innovation.
  • CEP's unique approach provides an opportunity to build the evidence base for multidomain lifestyle interventions and to develop and refine lifestyle biomarkers that can be used for early detection of MCI, tracking of disease progression, and objective measurement of the impact of lifestyle interventions.
非药物治疗方法的发展得到了证据的支持，即解决关键的可改变的风险因素可以预防或延迟高达45%的痴呆病例。查理和哈丽特·谢弗认知赋权项目（CEP）是为了解决目前在减少轻度认知障碍（MCI）患者生活方式风险因素和改善生活质量的干预措施的获取和证据方面的差距而开发的。与患者和家属、临床医生、研究人员和行业专业人士共同设计，CEP位于一个概念框架中，该框架指导评估和干预/支持，以全面解决MCI患者的生活体验。CEP包括四个核心（治疗方案、技术、建筑环境和创新加速器），它们映射到概念框架。我们认为，我们的方法提供了一个机会，为多领域生活方式项目的证据基础做出贡献，并对MCI以及个人如何管理它有了更深入的了解。认知赋权项目（CEP）是一个多领域的生活方式项目，使用共同设计过程和概念框架开发，全面解决轻度认知障碍（MCI）的生活体验。CEP通过映射到概念框架的四个核心提供全面的评估和干预/支持：治疗方案，技术，建筑环境和研究创新。CEP的独特方法为建立多领域生活方式干预的证据基础、开发和完善生活方式生物标志物提供了机会，这些生物标志物可用于MCI的早期检测、疾病进展的跟踪和生活方式干预影响的客观测量。
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引用次数: 0
Counteracting white matter injury to mitigate APOE 𝜀4-related ARIA 对抗白质损伤以减轻APOE𝜀4相关ARIA
IF 11.1 1区 医学 Q1 CLINICAL NEUROLOGY
Alzheimer's & Dementia
Pub Date : 2026-01-28 DOI: 10.1002/alz.71091
Yorito Hattori
<p>To the Editor:</p><p>The incidence and severity of amyloid-related imaging abnormalities (ARIA) are consistently higher in <i>apoelipoprotein E4 (APOE4)</i> carriers enrolled in anti-amyloid antibody trials, with the greatest risk observed in those with <i>APOE4</i> homozygosity. Mechanistically, apoE4 inherently undermines cerebrovascular integrity through direct injury to the neurovascular unit and the promotion of cerebral amyloid angiopathy. We previously showed that apoE4 drove the excessive production of cerebrovascular reactive oxygen species (ROS) and the resultant neurovascular dysfunction, including endothelial dysfunction and neurovascular uncoupling.<span><sup>1</sup></span> At the cellular level, border-associated macrophages (BAMs), i.e., myeloid cells closely opposed to neocortical microvessels, act as apoE4-dependent sources and effectors of nicotinamide adenine dinucleotide phosphate (NADPH)-oxidase-derived ROS, which impair neurovascular function.<span><sup>2</sup></span> In parallel, apoE4 activates the cyclophilin A–matrix metallopeptidase 9 pathway, amplifying inflammation and blood–brain barrier (BBB) disruption.<span><sup>3</sup></span> Chronic ROS and inflammation exposure converge on BBB breakdown through reduced tight junction integrity, diminished transendothelial electrical resistance, and basement membrane thinning.<span><sup>3-5</sup></span> Within the cerebral amyloid angiopathy axis, apoE4 increases the amyloid beta (Aβ)<sub>40</sub>/Aβ<sub>42</sub> ratio, favors vascular over parenchymal deposition, and slows the clearance of Aβ–apoE4 complexes across the BBB.<span><sup>6, 7</sup></span> Collectively, these pathways plausibly increase the risk of ARIA in <i>APOE4</i> carriers.</p><p>We read with great interest the article entitled “Independent effects of white matter lesion volume and <i>APOE</i> ɛ4 on ARIA-H in A4 Study” by Shirzadi <i>et al</i>.<span><sup>8</sup></span> This elegant study demonstrates that the risk of spontaneous hemorrhagic lesions is low in both homozygous and heterozygous <i>APOE4</i> carriers with low volume of white matter lesion, suggesting that ARIA is, at least in part, modifiable in <i>APOE4</i> carriers and that the risk of ARIA may be attenuated if white matter lesion burden is minimized before and during anti-amyloid therapy. Consistent with this view, in a secondary data analysis of the TRAILBLAZER-ALZ and ALZ-2 trials, mean arterial pressure < 93 mmHg with antihypertensive therapy independently predicted lower ARIA risk, whereas antidiabetic medications were associated with reduced risk in univariate analysis.<span><sup>9</sup></span> Hypertension and diabetes are leading drivers of white matter lesions; therefore, these data support the utility of strategies preserving cerebrovascular integrity in preventing ARIA. Additional common contributors to white matter lesions include smoking, atrial fibrillation, chronic kidney disease, obesity/metabolic syndrome, physical inactivit
致编者：在抗淀粉样蛋白抗体试验中，载脂蛋白E4 （APOE4）携带者的淀粉样蛋白相关成像异常（ARIA）的发生率和严重程度始终较高，APOE4纯合子携带者的风险最大。从机制上讲，apoE4通过直接损伤神经血管单位和促进脑淀粉样血管病而固有地破坏脑血管完整性。我们之前的研究表明，apoE4驱动了脑血管活性氧（ROS）的过量产生，并导致神经血管功能障碍，包括内皮功能障碍和神经血管解耦在细胞水平上，边界相关巨噬细胞（BAMs），即与新皮质微血管紧密对立的髓系细胞，作为apoe4依赖的烟酰胺腺嘌呤二核苷酸磷酸（NADPH）氧化酶衍生的ROS的来源和效应体，损害神经血管功能同时，apoE4激活亲环蛋白a -基质金属肽酶9通路，放大炎症和血脑屏障（BBB）破坏慢性ROS和炎症暴露会通过紧密连接完整性降低、跨内皮电阻降低和基底膜变薄导致血脑屏障破坏。3-5在脑淀粉样血管病轴中，apoE4增加淀粉样β (Aβ)40/Aβ42比值，有利于血管沉积而非实质沉积，并减缓Aβ - apoE4复合物在血脑屏障上的清除。我们饶有兴趣地阅读了Shirzadi等人发表的题为“A4研究中白质病变体积和APOE / 4对ARIA- h的独立影响”的文章。8这项优雅的研究表明，在白质病变体积小的纯合子和杂合子APOE4携带者中，自发出血性病变的风险都很低，这表明ARIA至少部分是：如果在抗淀粉样蛋白治疗前和治疗期间将白质病变负担降至最低，ARIA的风险可能会降低。与这一观点一致的是，在对TRAILBLAZER-ALZ和ALZ-2试验的二次数据分析中，抗高血压治疗的平均动脉压&lt； 93 mmHg独立预测较低的ARIA风险，而抗糖尿病药物在单变量分析中与降低风险相关高血压和糖尿病是白质病变的主要驱动因素；因此，这些数据支持保护脑血管完整性策略在预防ARIA中的效用。导致白质病变的其他常见因素包括吸烟、心房颤动、慢性肾病、肥胖/代谢综合征、缺乏身体活动、睡眠呼吸暂停和过量饮酒。因此，通过严格控制血压和血糖、戒烟、运动、优化睡眠、体重管理、适度饮酒、治疗房颤和睡眠呼吸暂停等多领域生活方式/血管干预，对启动抗淀粉样蛋白抗体的APOE4携带者可能特别有价值。翻译，apoe4导向的血管保护可以补充对危险因素的优化。首先，APOE4驱动sirtuin 1 （SIRT1）活性降低导致微血管内皮屏障功能障碍；因此，sirt1增强策略，包括生活方式调整和白藜芦醇，可以帮助血脑屏障稳定4，作为对抗apoe4诱导的微血管内皮细胞功能障碍的潜在策略，这有助于ARIA。其次，在BAMs中靶向抑制NADPH氧化酶，即gp91ds- that肽治疗，可降低ROS并使APOE4背景下的神经血管解耦和内皮功能障碍正常化2第三，实验中通过脑室/椎管内氯膦酸脂质体注射去除BAMs可减少脑血管ROS，改善体内神经血管功能。2,10虽然它们还没有准备好用于临床部署，后两种方法阐明了可处理的上游节点，即bamm衍生的ROS和内皮弹性，这可以通过更安全的药物方法来解决。 我们建议针对APOE4携带者正在进行的和未来的抗淀粉样蛋白试验和临床项目采取以下三个切实可行的步骤：根据白质病变负担对参与者进行基线分层和监测，通过结合白质高强度/病变的标准化量化来识别高风险个体并跟踪治疗后出现的变化；通过在抗淀粉样蛋白治疗过程中积极管理血压（适当时目标平均动脉压为93 mmHg）、糖尿病和其他白质病变危险因素，并提供依从性支持，制定了多领域血管护理方案；以及辅助血管保护策略，利用候选药物和生活方式/血管干预来增强内皮健康，例如那些针对sirt1相关途径的药物，并抑制脑血管氧化应激。总之，Shirzadi等人扩展了我们对apoe4相关ARIA的理解，指出通过最小化白质病变负担可以预防。再加上试验水平的信号表明，控制血管危险因素可以减轻ARIA，这些数据支持随机对照试验，测试多域生活方式/血管干预，并最终在APOE4携带者中，将血管保护佐剂与抗淀粉样蛋白抗体联合治疗。这些策略直接针对ARIA背后的血管病理，同时为那些遗传风险最大的人保留了改善疾病的治疗途径。作者声明无利益冲突。作者披露可在支持信息。
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引用次数: 0
Biomarkers in patients with clinical signs of mild cognitive impairment or mild Alzheimer's disease but without amyloid deposits on positron emission tomography: Results from Bio-Hermes Study participants 有轻度认知障碍或轻度阿尔茨海默病临床症状但在正电子发射断层扫描上没有淀粉样蛋白沉积的患者的生物标志物：来自Bio‐Hermes研究参与者的结果
IF 11.1 1区 医学 Q1 CLINICAL NEUROLOGY
Alzheimer's & Dementia
Pub Date : 2026-01-28 DOI: 10.1002/alz.71085
Richard C. Mohs, Douglas W. Beauregard, Lynne Hughes, Cyndy B. Cordell, Allan I. Levey, Saima Rathore, Nicholas T. Seyfried, Erik C. B. Johnson, Jessie Nicodemus-Johnson, Joshua Christensen, Robin Wolz, John Dwyer

INTRODUCTION

Alzheimer's disease (AD) study participants may present with cognitive impairment who do not have brain amyloid deposits (Aβ−). Identifying predictive biomarkers for non-amyloid-related CI may provide better screening tests for trials seeking only CI Aβ+ participants and new therapy targets.

METHODS

Analysis of the Bio-Hermes biomarker database identified subpopulations of clinically normal, CN Aβ− (n = 313), CI Aβ− (n = 296), and CI Aβ+ (n = 258), and CN Aβ+ (n = 84) participants. Comparative analysis of demographics, clinical assessments, biomarkers, cytokines, and proteomics results was conducted.

RESULTS

Subgroup comparison of CI Aβ− versus CN Aβ− found that neurofilament light most clearly differentiated CI Aβ− from CN Aβ− participants. No other biomarker analysis reached a level of differential significance.

DISCUSSION

Analyses showed many novel biomarkers do not differentiate CI Aβ− from CN Aβ−. New biomarkers are needed to best determine the neuropathology of the clinical presentation of AD.

Highlights

  • NfL differentiated CN Aβ− versus cognitively impaired Aβ−.
  • Proteomics (two platforms) did not differentially assess cognitively impaired Aβ−-.
  • Many novel biomarkers did not differentially assess cognitively impaired Aβ−.
  • New biomarkers are needed to determine the neuropathology of AD clinical presentation.
阿尔茨海默病（AD）研究的参与者可能表现为认知障碍，但他们没有脑淀粉样蛋白沉积（Aβ−）。鉴定非淀粉样蛋白相关CI的预测性生物标志物可能为仅寻求CI Aβ+参与者和新治疗靶点的试验提供更好的筛选试验。方法对Bio - Hermes生物标志物数据库进行分析，确定临床正常、CN Aβ - (n = 313)、CI Aβ - (n = 296)、CI Aβ+ (n = 258)和CN Aβ+ (n = 84)参与者亚群。进行了人口统计学、临床评估、生物标志物、细胞因子和蛋白质组学结果的比较分析。结果CI Aβ -与CN Aβ -的亚组比较发现，神经丝光最明显地将CI Aβ -与CN Aβ -参与者区分开来。其他生物标志物分析均未达到差异显著性水平。分析表明，许多新的生物标志物不能区分CI Aβ−和CN Aβ−。需要新的生物标志物来最好地确定阿尔茨海默病临床表现的神经病理学。NfL分化CN Aβ -与认知受损的Aβ -。蛋白质组学（两种平台）对认知受损的Aβ−‐的评估没有差异。许多新的生物标志物对认知受损的Aβ−没有差异评估。需要新的生物标志物来确定阿尔茨海默病临床表现的神经病理学。
{"title":"Biomarkers in patients with clinical signs of mild cognitive impairment or mild Alzheimer's disease but without amyloid deposits on positron emission tomography: Results from Bio-Hermes Study participants","authors":"Richard C. Mohs,&nbsp;Douglas W. Beauregard,&nbsp;Lynne Hughes,&nbsp;Cyndy B. Cordell,&nbsp;Allan I. Levey,&nbsp;Saima Rathore,&nbsp;Nicholas T. Seyfried,&nbsp;Erik C. B. Johnson,&nbsp;Jessie Nicodemus-Johnson,&nbsp;Joshua Christensen,&nbsp;Robin Wolz,&nbsp;John Dwyer","doi":"10.1002/alz.71085","DOIUrl":"10.1002/alz.71085","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> INTRODUCTION</h3>\u0000 \u0000 <p>Alzheimer's disease (AD) study participants may present with cognitive impairment who do not have brain amyloid deposits (Aβ−). Identifying predictive biomarkers for non-amyloid-related CI may provide better screening tests for trials seeking only CI Aβ+ participants and new therapy targets.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> METHODS</h3>\u0000 \u0000 <p>Analysis of the Bio-Hermes biomarker database identified subpopulations of clinically normal, CN Aβ− (<i>n = </i>313), CI Aβ− (<i>n</i> = 296), and CI Aβ+ (<i>n =</i> 258), and CN Aβ+ (<i>n = </i>84) participants. Comparative analysis of demographics, clinical assessments, biomarkers, cytokines, and proteomics results was conducted.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> RESULTS</h3>\u0000 \u0000 <p>Subgroup comparison of CI Aβ− versus CN Aβ− found that neurofilament light most clearly differentiated CI Aβ− from CN Aβ− participants. No other biomarker analysis reached a level of differential significance.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> DISCUSSION</h3>\u0000 \u0000 <p>Analyses showed many novel biomarkers do not differentiate CI Aβ− from CN Aβ−. New biomarkers are needed to best determine the neuropathology of the clinical presentation of AD.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Highlights</h3>\u0000 \u0000 <div>\u0000 <ul>\u0000 \u0000 <li>NfL differentiated CN Aβ− versus cognitively impaired Aβ−.</li>\u0000 \u0000 <li>Proteomics (two platforms) did not differentially assess cognitively impaired Aβ−-.</li>\u0000 \u0000 <li>Many novel biomarkers did not differentially assess cognitively impaired Aβ−.</li>\u0000 \u0000 <li>New biomarkers are needed to determine the neuropathology of AD clinical presentation.</li>\u0000 </ul>\u0000 </div>\u0000 </section>\u0000 </div>","PeriodicalId":7471,"journal":{"name":"Alzheimer's & Dementia","volume":"22 1","pages":""},"PeriodicalIF":11.1,"publicationDate":"2026-01-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://alz-journals.onlinelibrary.wiley.com/doi/epdf/10.1002/alz.71085","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146070689","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Multi-omic expression of the VEGF family relates to Alzheimer's disease across diverse populations VEGF家族的多组学表达与不同人群的阿尔茨海默病有关。
IF 11.1 1区 医学 Q1 CLINICAL NEUROLOGY
Alzheimer's & Dementia
Pub Date : 2026-01-28 DOI: 10.1002/alz.71100
Julia B. Libby, Kacie D. Deters, Nilüfer Ertekin-Taner, Minerva M. Carrasquillo, Mariet Allen, Philip De Jager, Vilas Menon, Bin Zhang, Vahram Haroutunian, Allan I. Levey, Nicholas T. Seyfried, Rima Kaddurah-Daouk, Steve Finkbeiner, Daifeng Wang, Anna K. Greenwood, Abby Vander Linden, Laura Heath, William L. Poehlman, Logan Dumitrescu, Vladislav A. Petyuk, David A. Bennett, Julie A. Schneider, Lisa L. Barnes, Timothy J. Hohman

INTRODUCTION

The vascular endothelial growth factor (VEGF) signaling family plays a role in neurodegenerative diseases, including Alzheimer's disease (AD). Previous work has shown widespread effects of the members FLT1, FLT4, and VEGFB on AD outcomes. However, these analyses have focused within the non-Hispanic White (NHW) population.

NETHODS

The goal of this study was to analyze the effects of the VEGF family in underrepresented populations, leveraging large and diverse bulk RNA sequencing and tandem mass tag–mass spectrometry (TMT-MS) proteomic data. Outcomes included measures of AD pathology and diagnosis.

RESULTS

Within underrepresented populations, we replicated previously reported effects of FLT1 and FLT4, whereby higher protein abundance was observed in the AD brain and was associated with higher neuropathology burden. In stratified analyses, these associations were largely consistent across race and ethnicity.

DISCUSSION

This multi-omic study on the role of the VEGF family in AD emphasizes the need for more representative studies focused on therapeutic targets for AD.

Highlights

  • Vascular endothelial growth factor (VEGF) genes and proteins were quantified in four different brain regions. Samples included participants from four different populations.
  • Previously observed effects were replicated in diverse populations.
  • This study is the largest multi-omic study of the vascular endothelial growth factor (VEGF) genes among Alzheimer's disease (AD) participants from diverse populations.
血管内皮生长因子（VEGF）信号家族在包括阿尔茨海默病（AD）在内的神经退行性疾病中发挥作用。先前的研究表明，FLT1、FLT4和VEGFB成员对AD的预后有广泛的影响。然而，这些分析主要集中在非西班牙裔白人（NHW）人群中。方法：本研究的目的是分析VEGF家族在代表性不足的人群中的作用，利用大量和多样化的散装RNA测序和串联质谱标记-质谱（TMT-MS）蛋白质组学数据。结果包括AD病理和诊断指标。结果：在代表性不足的人群中，我们重复了先前报道的FLT1和FLT4的作用，即在AD大脑中观察到更高的蛋白质丰度，并与更高的神经病理学负担相关。在分层分析中，这些关联在种族和民族之间基本一致。讨论：这项关于VEGF家族在AD中的作用的多组学研究强调了对AD的治疗靶点进行更多有代表性的研究的必要性。重点：血管内皮生长因子（VEGF）基因和蛋白在四个不同的脑区域被量化。样本包括来自四个不同人群的参与者。先前观察到的效果在不同的人群中得到了重复。这项研究是对不同人群阿尔茨海默病（AD）参与者血管内皮生长因子（VEGF）基因进行的最大的多组学研究。
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引用次数: 0
CTE neuropathology alone is associated with dementia and cognitive symptoms CTE神经病理学本身与痴呆和认知症状有关
IF 11.1 1区 医学 Q1 CLINICAL NEUROLOGY
Alzheimer's & Dementia
Pub Date : 2026-01-27 DOI: 10.1002/alz.71032
Rachael M. Layden, Jenna R. Groh, Annalise E. Miner, Abigail Kidd, Sophia B. Nosek, Stephanie Gonzalez Gil, Bobak Abdolmohammadi, Steven Lenio, Christopher J. Nowinski, Yorghos Tripodis, Brett M. Martin, Joseph N. Palmisano, Brigid C. Dwyer, Douglas I. Katz, Lee E. Goldstein, Robert C. Cantu, Robert A. Stern, Thor D. Stein, Ann C. McKee, Daniel H. Daneshvar, Jesse Mez, Michael L. Alosco

INTRODUCTION

This studyexamined the independent contribution of chronic traumatic encephalopathy (CTE) neuropathology to symptoms.

METHODS

The sample included 614 brain donors with (n = 366) and without (n = 248) autopsy-confirmed CTE. Brain donors with other major neurodegenerative disease diagnoses were excluded. Informants completed cognitive and neuropsychiatric measures. Dementia was determined during diagnostic consensus conferences.

RESULTS

CTE stage IV (of IV) was associated with 4.48 (95% confidence interval [CI] = 1.97–10.90) increased odds of having dementia. CTE stage III had an odds ratio of 2.12 (95% CI = 1.91–3.77). Higher CTE stage was associated with greater informant-reported cognitive symptoms (p < 0.01). There were no associations with mood/behavioral scales.

DISCUSSION

CTE stage III/IV neuropathology was associated with dementia and cognitive symptoms: those with stage IV were 4.5 times more likely to have dementia than those without CTE. It is uncertain if low-stage CTE clinically manifests, and mood/behavioral symptoms likely have multifactorial causes and/or a fluctuating course.

Highlights

  • Stage III and IV chronic traumatic encephalopathy (CTE) are independently associated with increased odds of having dementia.
  • Higher CTE stage was associated with greater informant-reported cognitive symptoms.
  • Stage I and II CTE were not associated with cognitive symptoms or dementia.
  • CTE of any severity was not associated with informant-reported mood or behavioral symptoms.
本研究考察了慢性创伤性脑病（CTE）神经病理学对症状的独立贡献。
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引用次数: 0
Correction to “Evaluating linked ICD-10 Medicare claims data as a method of dementia case ascertainment in research settings” 对“评估ICD-10相关医疗保险索赔数据作为研究环境中痴呆病例确定方法”的更正
IF 11.1 1区 医学 Q1 CLINICAL NEUROLOGY
Alzheimer's & Dementia
Pub Date : 2026-01-26 DOI: 10.1002/alz.71161
<p>Bhattacharyya J, Barnes LL, Chen Y, et al. Evaluating linked ICD-10 Medicare claims data as a method of dementia case ascertainment in research settings. <i>Alzheimers Dement</i>. 2025;21(5):e70200. doi:10.1002/alz.70200</p><p>In the paper by Bhattacharyya et al. (Evaluating linked ICD-10 Medicare claims data as a method of dementia case ascertainment in research settings. <i>Alzheimers Dement</i>. 2025; 21:e70200. https://doi.org/10.1002/alz.70200), we identified errors requiring correction: an error in the early part of our coding which resulted in small changes in the performance metrics and regression model coefficients presented in the article, an error in the coding of the lookback period for one of the code definitions (Bynum Standard), and an error in our reporting citing use of a standard 1-year lookback rather than a standard 3-year lookback.</p><p>The overall conclusions of the paper did not change, although some details of the performance metrics did.</p><p>The authors regret these errors. We detail necessary changes to the text here and have reissued corrected versions of Tables 3–6 below, reflecting changes to performance metrics and regression model coefficients.</p><p>In the initial publication of this article, there is an erroneous statement in the Results section of the abstract, which reads: <i>“Accuracy of ICD-10 code definitions was high (87%–90%); 5 of 6 code definitions favored specificity over sensitivity.”</i> The corrected sentence should read<i>: “Accuracy of ICD-10 code definitions was high (86%–92%); all code definitions favored specificity over sensitivity.”</i></p><p>In the initial publication of this article, there is an erroneous statement at the end of Section 2.5, which reads: “All available Medicare FFS claims data from the 12-month period (± 6 months) surrounding a study visit were used to determine participants’ dementia status … we used a standard 1-year lookback period for all code definitions in analyses so that we could make direct comparisons.” The corrected sentence should read: “All available Medicare FFS claims data from the 36-month period prior to the study visit were used to determine participants’ dementia … we used a standard 3-year lookback period for all code definitions in analyses so that we could make direct comparisons.”</p><p>Similarly, there is an erroneous sentence included in the footnote of Table 1, which reads: <i>“Our analysis used a reference period of 1 year surrounding the index date.”</i> The corrected footnote should read: <i>“Our analysis used a reference period of 3 years prior to the index date.”</i></p><p>Section 3.2 requires updates reflecting updated numbers reported in Table 3 and should be replaced with the following:</p><p><i>“Table</i> 3 <i>shows performance metrics for each ICD-10 dementia code definition, overall and by subgroups. All 6 code definitions show similar overall accuracy (range: 86%–92%) and NPV (range: 94%–96%) compared to the RADC research standard.
巴塔查里亚J， Barnes LL，陈勇，等。评估相关ICD-10医疗保险索赔数据作为痴呆病例确定研究设置的方法。阿尔茨海默病。2025;21(5):e70200。doi: 10.1002 / alz。[70200]在Bhattacharyya等人的论文中（评估ICD-10医疗保险索赔数据作为研究环境中痴呆病例确定的方法）。阿尔茨海默病。2025；21: e70200。https://doi.org/10.1002/alz.70200)，我们发现了需要纠正的错误：编码早期的一个错误导致了文章中给出的性能指标和回归模型系数的微小变化，其中一个代码定义（Bynum标准）的回顾周期编码中的一个错误，以及我们报告中引用标准1年回顾而不是标准3年回顾的错误。论文的总体结论没有改变，尽管绩效指标的一些细节发生了变化。作者对这些错误感到遗憾。我们在这里详细说明了对文本的必要更改，并重新发布了下面表3-6的更正版本，以反映性能指标和回归模型系数的更改。在本文最初发表时，摘要的Results部分有一个错误的陈述：“ICD-10代码定义的准确率很高（87%-90%）；6个代码定义中有5个更倾向于特异性而不是敏感性。”更正后的句子应该是：“ICD-10代码定义的准确性很高（86%-92%）；所有的代码定义都倾向于特异性而不是敏感性。”在这篇文章的最初发表中，在2.5节的末尾有一个错误的声明：“所有可用的医疗保险FFS数据都是在研究访问的12个月（±6个月）期间用于确定参与者的痴呆状态……我们在分析中对所有代码定义使用了标准的1年回顾期，以便我们可以进行直接比较。”更正后的句子应该是：“在研究访问之前的36个月期间，所有可用的医疗保险FFS索赔数据都用于确定参与者的痴呆症……我们在分析中对所有代码定义使用了标准的3年回顾期，以便我们可以进行直接比较。”同样，在表1的脚注中包含了一个错误的句子：“我们的分析使用了索引日期周围1年的参考期。”更正后的脚注应该是：“我们的分析使用了索引日期之前3年的参考期。”第3.2节要求更新反映表3中报告的更新数字，并应替换为以下内容：“表3显示了每个ICD-10痴呆代码定义的总体和子组的性能指标。与RADC研究标准相比，所有6个代码定义显示出相似的总体准确性（范围：86%-92%）和净现值（范围：94%-96%）。所有六种代码定义都以较低的灵敏度为代价具有高特异性。当在子组中评估性能指标时，结果是相似的。所有代码定义在子组中都显示出相似的准确性，所有代码定义都倾向于特异性而不是敏感性，Moura等人（2021）和NORC高度可能和可能（2024）代码定义的性能指标非常接近或相同。”“然而，尽管各子组算法的性能相似，但无论哪种算法，子组之间的性能差异很大。例如，准确率范围从75%到98%，NPV范围从85%到99%。与其他亚组相比，年龄较小的亚组（80岁以下）具有最高的准确性（范围：95%-98%）和最高的NPV（范围：99%-99%），但该组的PPV也最低（范围：15%-31%）。有卒中史的亚组准确率最低（范围：75%-83%），NPV最低（范围：85%-88%）。3.3节中的以下内容应省略，以反映对表5的更新：“虽然少数民族种族与假阳性分类之间的关联大大提高，但仅在观察到的一半代码定义中显着或略微显着。”最后，讨论中的以下句子应该省略：“考虑的所有ICD-10代码定义对于RADC痴呆分类具有相似的准确性（87%-90%）和NPV（96%-98%）。除了拜纳姆标准外，大多数人更倾向于特异性而不是敏感性，该标准的灵敏度更高，但特异性略低。要符合使用拜纳姆标准的痴呆标准，参与者必须至少有一份来自MedPAR（即住院或熟练护理机构）、家庭健康或临终关怀档案的符合条件的ICD-10代码的索赔，或至少有两份来自载体或门诊档案的符合条件的ICD-10代码的索赔（间隔至少7天）。这些标准可能使Bynum标准ICD-10代码定义的灵敏度更高。 并替换为以下内容：“考虑的所有ICD-10代码定义对于RADC痴呆分类具有相似的准确性（86%-92%）和NPV（94%-96%）。所有人都倾向于特异性而非敏感性。”我们为这个错误道歉。表3。与2015年10月至2019年12月拉什阿尔茨海默病中心标准相比，ICD-10代码定义的3年回顾绩效指标，总体和按亚组分列。准确度灵敏度规格ppvnpvradc痴呆状态患病率总体0.09 ccw0.890.610.910.420.96 bynum Standard0.920.570.950.540.96Moura等人0.900.610.930.480.96 jain等人0.920.430.970.610.94 norc Highly Likely and Likely0.900.610.930.480.96 norc Highly Likely, Likely和probly0.860.640.890.360.96 age年龄较小（&lt; 80） 0.010年龄较大（≥80）0.14 ccw0.960.610.960.180.990.0.850.610.880.460.93 bynum Standard0.980.480.980.270.990.880.570.930.570.93Moura et al.0.960.580.970.210.990.870.610.910.520.93Jain et al. 0.980.290.990.0.30.310.990.890.440.960.630.91 norc Highly Likely, Likely, LikelyProbably0.950.650.950.150.990.810.640.840.400.94EducationLower教育高等教育(& lt; 16) 0.09(≥16)0.10 ccw0.870.630.890.350.960.900.610.930.480.96bynum Standard0.910.570.940.460.960.920.560.960.590.95Moura et al.0.890.620.910.400.960.910.600.940.530.96Jain et al.0.930.470.970.580.950.920.420.970.620.94NORC极有可能和Likely0.890.620.910.400.960.910.600.940.530.96NORC极有可能,有可能的是,和Probably0.840.650.860.300.960.880.640.900.410.96SexMale0.09Female0.09CCW0.880.590.910.380.960.890.620.920.440.96Bynum Standard0.910.530.940.470.950.920.580.950.560.96Moura et al.0.890.570.920.410.960.910.620.940.500.96Jain et al.0.910.330.970.490.940.920.460.970.630.95NORC极有可能和Likely0.890.570
{"title":"Correction to “Evaluating linked ICD-10 Medicare claims data as a method of dementia case ascertainment in research settings”","authors":"","doi":"10.1002/alz.71161","DOIUrl":"10.1002/alz.71161","url":null,"abstract":"&lt;p&gt;Bhattacharyya J, Barnes LL, Chen Y, et al. Evaluating linked ICD-10 Medicare claims data as a method of dementia case ascertainment in research settings. &lt;i&gt;Alzheimers Dement&lt;/i&gt;. 2025;21(5):e70200. doi:10.1002/alz.70200&lt;/p&gt;&lt;p&gt;In the paper by Bhattacharyya et al. (Evaluating linked ICD-10 Medicare claims data as a method of dementia case ascertainment in research settings. &lt;i&gt;Alzheimers Dement&lt;/i&gt;. 2025; 21:e70200. https://doi.org/10.1002/alz.70200), we identified errors requiring correction: an error in the early part of our coding which resulted in small changes in the performance metrics and regression model coefficients presented in the article, an error in the coding of the lookback period for one of the code definitions (Bynum Standard), and an error in our reporting citing use of a standard 1-year lookback rather than a standard 3-year lookback.&lt;/p&gt;&lt;p&gt;The overall conclusions of the paper did not change, although some details of the performance metrics did.&lt;/p&gt;&lt;p&gt;The authors regret these errors. We detail necessary changes to the text here and have reissued corrected versions of Tables 3–6 below, reflecting changes to performance metrics and regression model coefficients.&lt;/p&gt;&lt;p&gt;In the initial publication of this article, there is an erroneous statement in the Results section of the abstract, which reads: &lt;i&gt;“Accuracy of ICD-10 code definitions was high (87%–90%); 5 of 6 code definitions favored specificity over sensitivity.”&lt;/i&gt; The corrected sentence should read&lt;i&gt;: “Accuracy of ICD-10 code definitions was high (86%–92%); all code definitions favored specificity over sensitivity.”&lt;/i&gt;&lt;/p&gt;&lt;p&gt;In the initial publication of this article, there is an erroneous statement at the end of Section 2.5, which reads: “All available Medicare FFS claims data from the 12-month period (± 6 months) surrounding a study visit were used to determine participants’ dementia status … we used a standard 1-year lookback period for all code definitions in analyses so that we could make direct comparisons.” The corrected sentence should read: “All available Medicare FFS claims data from the 36-month period prior to the study visit were used to determine participants’ dementia … we used a standard 3-year lookback period for all code definitions in analyses so that we could make direct comparisons.”&lt;/p&gt;&lt;p&gt;Similarly, there is an erroneous sentence included in the footnote of Table 1, which reads: &lt;i&gt;“Our analysis used a reference period of 1 year surrounding the index date.”&lt;/i&gt; The corrected footnote should read: &lt;i&gt;“Our analysis used a reference period of 3 years prior to the index date.”&lt;/i&gt;&lt;/p&gt;&lt;p&gt;Section 3.2 requires updates reflecting updated numbers reported in Table 3 and should be replaced with the following:&lt;/p&gt;&lt;p&gt;&lt;i&gt;“Table&lt;/i&gt; 3 &lt;i&gt;shows performance metrics for each ICD-10 dementia code definition, overall and by subgroups. All 6 code definitions show similar overall accuracy (range: 86%–92%) and NPV (range: 94%–96%) compared to the RADC research standard. ","PeriodicalId":7471,"journal":{"name":"Alzheimer's & Dementia","volume":"22 1","pages":""},"PeriodicalIF":11.1,"publicationDate":"2026-01-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://alz-journals.onlinelibrary.wiley.com/doi/epdf/10.1002/alz.71161","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146048817","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Racial, ethnic and sex-specific mechanisms of obstructive sleep apnea and Alzheimer's disease risk 阻塞性睡眠呼吸暂停和阿尔茨海默病风险的种族、民族和性别特异性机制。
IF 11.1 1区 医学 Q1 CLINICAL NEUROLOGY
Alzheimer's & Dementia
Pub Date : 2026-01-26 DOI: 10.1002/alz.71144
Komal Patel Murali, Joshua Gills, Arlener Turner, Anthony Briggs, Mark Bernard, Elena Valkanova, Alfred K. Mbah, Ogie Queen Umasabor-Bubu, Glenna Brewster, Zainab Osakwe, Natasha Williams, Clemma Muller, Dayna A. Johnson, Chinedu T. Udeh-Momoh, Olugbenga Ogedegbe, Indu Ayappa, Ricardo Osorio, Girardin Jean-Louis, Alberto R. Ramos, Omonigho Michael Bubu

BACKGROUND

Obstructive sleep apnea (OSA) is associated with Alzheimer's disease (AD) risk. Racial-, ethnic-, and sex-specific mechanisms of OSA and AD risk were examined.

METHODS

We analyzed data from 3978 polysomnography patients without cognitive decline aged ≥ 60 including 663 OSA+ patients (284 non-Hispanic White, 207 Black, 172 Hispanic) matched to OSA– cohorts (1:1, n = 663; 1:4, n = 2652) and followed for AD through 2013.

RESULTS

During the 8.5 (standard deviation 1.4) year period, 358 patients developed AD. AD risk was higher for Black (adjusted hazard ratio [aHR] 2.24 [1.24–2.71]), Hispanic (aHR 1.73, [1.38–3.51]), White (aHR 1.83, [1.21–3.37]), male (aHR 2.38, [1.31–3.47]), and female (aHR 1.37, [1.14–2.41]) patients. Hypoxia, sleep fragmentation, and sleep duration (p < 0.01) were associated with increased risk. Black and Hispanic, and female patients showed stronger effects for hypoxia and duration, and fragmentation, respectively.

DISCUSSION

Hypoxia, fragmentation, and duration may underlie racial-, ethnic-, and sex-specific effects of AD risk.

背景：阻塞性睡眠呼吸暂停（OSA）与阿尔茨海默病（AD）风险相关。研究了OSA和AD风险的种族、民族和性别特异性机制。方法：我们分析了3978例年龄≥60岁无认知能力下降的多道睡眠检查患者的数据，其中663例OSA+患者（284例非西班牙裔白人，207例黑人，172例西班牙裔）与OSA队列（1:1,n = 663; 1:4, n = 2652）匹配，并随访至2013年AD。结果：在8.5年（标准差1.4）期间，358例患者发生AD。黑人（校正危险比[aHR] 2.24[1.24-2.71]）、西班牙裔（aHR 1.73,[1.38-3.51]）、白人（aHR 1.83,[1.21-3.37]）、男性（aHR 2.38,[1.31-3.47]）和女性（aHR 1.37,[1.14-2.41]）患者的AD风险较高。缺氧、睡眠片段和睡眠持续时间(p讨论：缺氧、睡眠片段和睡眠持续时间可能是AD风险的种族、民族和性别特异性影响的基础。
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引用次数: 0
Evaluation of ASC as a therapeutic target for Alzheimer's disease ASC作为阿尔茨海默病治疗靶点的评价
IF 11.1 1区 医学 Q1 CLINICAL NEUROLOGY
Alzheimer's & Dementia
Pub Date : 2026-01-25 DOI: 10.1002/alz.71104
W. Brent Clayton, Joshua A. Kulas, Jiahui Liu, Nidhi Walia, Claudia Rangel-Barajas, Travis Johnson, Jie Zhang, Kun Huang, Andrew D. Mesecar, Jeffrey L. Dage, Bruce T. Lamb, Alan D. Palkowitz, Timothy I. Richardson

Neuroinflammation is increasingly recognized as a central contributor to the pathogenesis and progression of Alzheimer's disease (AD). The apoptosis-associated speck-like protein containing a CARD (ASC), encoded by the PYCARD gene, plays a critical role in the formation of multiple inflammasomes, including NLRP3, a key mediator of inflammation signaling. Beyond its role in inflammasome formation, extracellular ASC specks have been shown to promote amyloid-β aggregation, showing a potential link between inflammation and plaque formation. In this review, we examine the role of ASC in AD pathology and highlight emerging tools to study ASC biology and strategies for ASC targeted drug discovery.

神经炎症越来越被认为是阿尔茨海默病（AD）发病和进展的核心因素。由PYCARD基因编码的含有CARD的凋亡相关斑点样蛋白（ASC）在多种炎症小体的形成中起关键作用，包括NLRP3，这是炎症信号传导的关键介质。除了在炎性体形成中的作用外，细胞外ASC斑点已被证明可促进淀粉样蛋白- β聚集，显示炎症和斑块形成之间的潜在联系。在这篇综述中，我们探讨了ASC在AD病理中的作用，并重点介绍了研究ASC生物学的新兴工具和ASC靶向药物发现的策略。
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引用次数: 0
Author's response to letter to the editor: “How culture shapes subjective cognitive decline reporting: Refining assessment tools with digital solutions” 作者对致编辑的信的回复：“文化如何塑造主观认知衰退报告：用数字解决方案改进评估工具”
IF 11.1 1区 医学 Q1 CLINICAL NEUROLOGY
Alzheimer's & Dementia
Pub Date : 2026-01-25 DOI: 10.1002/alz.71139
Sarah Tomaszewski Farias
<p>We are excited that our paper entitled “Subjective cognitive decline among diverse older adults: Prevalence and associations with objective cognition”<span><sup>1</sup></span> has generated interest in how the expression of subjective cognitive decline (SCD) may be influenced by the lens of one's cultural background. We thank Drs. Rong Sun and Deqi Kong for comments in their Letter to the Editor and hope that this interchange will lead to additional impactful work on this important topic. In our paper, which leveraged baseline data from the cognitively healthy but at-risk cohort enrolled in the U.S. POINTER Trial, we examined the prevalence of SCD and associations between subjective and objective cognition across three ethnic and racial groups (African American/Black, Hispanic/Latino, and Non-Hispanic White [NHW] participants). Our study found that Hispanic/Latino participants were more likely to report SCD than NHW or African American/Black participants. However, significant associations between SCD ratings and objective cognitive function were observed primarily in NHW participants. Among African American/Black participants, SCD ratings correlated with objective cognitive function in one of three specific neuropsychological domains (processing speed). No association was found among Hispanic/Latino participants. A major impetus for our study was to contribute to the limited but growing body of work seeking to better understand potential differences in SCD across diverse groups. The impact of cultural background on the expression of various symptoms, the meaning and interpretation attributed to those symptoms, and whether and how treatment is sought have been described in other areas of medicine, particularly in reference to mental health.<span><sup>2</sup></span> In this context, it is not surprising that the same should be expected to be applicable to SCD.</p><p>Utilization of digital or other disease biomarkers (which can also be influenced by demographic factors) will undoubtedly be increasingly important for early disease detection. However, we believe that better understanding how culture shapes an individual's experience of cognitive aging, and the factors that contribute to its expression, remains a meaningful question and will contribute to more personalized care. This will, indeed, require continued advancements in the measurement of SCD aimed at better tailoring assessment to specific populations. This should include explicitly employing test development and validation methods to ensure the content and wording of items comprising SCD questionnaires are culturally relevant to the target population. For example, when developing an updated version of the Everyday Cognition (ECog) scales,<span><sup>3</sup></span> we interviewed a diverse group of older adults and their care partners to evaluate the perceived importance of each item and its relevance to daily life. Such information was then used to inform instrument revisions. Similar pe
我们很高兴我们题为“不同老年人的主观认知能力下降：患病率及其与客观认知的关联”的论文引起了人们对主观认知能力下降（SCD）的表达如何受到一个人的文化背景的影响的兴趣。我们感谢dr。请孙荣和孔德奇在给编辑的信中发表意见，并希望这次交流能在这一重要话题上产生更多有影响力的工作。在我们的论文中，我们利用了美国POINTER试验中认知健康但有风险的队列的基线数据，研究了三个民族和种族群体（非裔美国人/黑人、西班牙裔/拉丁裔和非西班牙裔白人[NHW]参与者）中SCD的患病率和主观认知与客观认知之间的关系。我们的研究发现西班牙裔/拉丁裔参与者比非裔美国人/黑人参与者更有可能报告SCD。然而，SCD评分与客观认知功能之间的显著关联主要在NHW参与者中观察到。在非裔美国人/黑人参与者中，SCD评分与三个特定神经心理学领域（处理速度）之一的客观认知功能相关。在西班牙裔/拉丁裔参与者中没有发现关联。我们研究的主要动力是为有限但不断增长的工作做出贡献，以更好地了解不同群体中SCD的潜在差异。文化背景对各种症状表现的影响、这些症状的含义和解释，以及是否和如何寻求治疗，在其他医学领域，特别是在精神健康方面都有描述在这种情况下，预计同样适用于SCD也就不足为奇了。利用数字或其他疾病生物标志物（也可能受到人口因素的影响）无疑将对早期疾病检测越来越重要。然而，我们相信，更好地理解文化如何塑造个人认知衰老的经历，以及促进其表达的因素，仍然是一个有意义的问题，并将有助于更个性化的护理。这确实需要在衡量可持续发展能力方面不断取得进展，以便更好地针对特定人群进行评估。这应该包括明确地采用测试开发和验证方法，以确保组成SCD问卷的项目的内容和措辞在文化上与目标人群相关。例如，在开发日常认知（ECog）量表的更新版本3时，我们采访了一组不同的老年人及其护理伙伴，以评估每个项目的感知重要性及其与日常生活的相关性。这些资料随后被用于通知文书的修订。类似的以人为中心的迭代测试开发方法可能有助于进一步扩展和开发新的SCD工具。单一的SCD工具可能不适合所有人群，尽管在特定文化的工具之间确定连接项目可能会实现协调。我们还试图使用差分项目函数（DIF）明确评估不同群体测量偏差对ECog的潜在影响虽然我们发现DIF的影响相对较小，并且在比较DIF调整和未调整的ECog评分时，ECog与认知或结构脑成像之间的关联没有显著差异，但在这一领域的更多工作显然是有必要的，并且应该纳入来自更广泛人群的数据。其他重要的问题仍然存在，可能也与更好地理解SCD在不同群体中的差异有关。在SCD领域的工作主要集中在记忆抱怨，但相对较少的工作已经做了检查SCD的其他表型。在我们的研究中，我们发现执行关注（与注意力分散有关）主要与处理速度认知领域有关。这种SCD表型最终可能与包括脑血管疾病在内的不同潜在疾病机制有关，5并可能有助于解释已观察到的不同群体的主观抱怨和疾病标志物之间的一些不同关联模式SCD也有一些特定的特征，比如担心/担心认知变化（有时被称为SCD +），这可能会增加发生认知障碍/痴呆的风险这些特征尚未在不同文化中得到很好的研究，但可能会改善不同群体的早期疾病检测。最后，虽然我们在比较主观认知和客观认知时基本上将神经心理测试表现视为“金标准”，但众所周知，神经心理测试表现受到各种人口因素的强烈影响。
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引用次数: 0
Overnight sleep affects the stability of neuropsychological classification in mild cognitive impairment 夜间睡眠影响轻度认知障碍患者神经心理分类的稳定性
IF 11.1 1区 医学 Q1 CLINICAL NEUROLOGY
Alzheimer's & Dementia
Pub Date : 2026-01-25 DOI: 10.1002/alz.71128
Jun Ha Chang, Gavin J. Latona, Matthew Rizzo, Vaishali Phatak, Daniel L. Murman

INTRODUCTION

Reversion to normal cognition in mild cognitive impairment (MCI) is relatively common. This study tested whether total sleep time (TST) and sleep efficiency (SE) on the night before cognitive testing predicts MCI reversion.

METHODS

Fifty-eight community-dwelling older adults with MCI (mean age = 75 years) participated. MCI was defined as cognitive performance ≥ 1.5 standard deviation below norms in at least one domain, with preserved daily functioning. Participants completed cognitive testing at baseline and 1-year follow-up, and sleep was objectively measured using actigraphy at baseline. Logistic regression assessed whether prior-night TST and SE predicts reversion, adjusting for age and sex.

RESULTS

Sixteen participants (27.6%) reverted. Shorter prior-night TST was associated with higher odds of reversion, whereas SE showed no significant association. Random night or chronic sleep measures showed no associations.

DISCUSSION

Acute sleep disruption may transiently impair cognition and contribute to MCI misclassification. Sleep screening before testing may improve diagnostic reliability.

Highlights

  • Shorter total sleep time on the night before cognitive testing was associated with higher odds of mild cognitive impairment (MCI) reversion after 1 year.
  • Sleep efficiency, random-night sleep, and 14-day average sleep showed no significant association with MCI reversion.
  • Single-domain MCI cases were more likely to revert than multi-domain MCI cases, suggesting greater susceptibility to acute factors such as poor sleep.
  • Brief screening of prior-night sleep or actigraphy-derived metrics could help identify low-reliability assessment and improve diagnostic stability in MCI research.
在轻度认知障碍（MCI）中恢复正常认知是比较常见的。本研究测试了认知测试前一晚的总睡眠时间（TST）和睡眠效率（SE）是否能预测轻度认知障碍的逆转。方法参与了58名社区居住的老年轻度认知障碍患者（平均年龄= 75岁）。轻度认知障碍被定义为至少在一个领域的认知表现低于标准1.5标准差，并保留日常功能。参与者在基线时完成认知测试和1年随访，并在基线时使用活动记录仪客观测量睡眠。在调整年龄和性别后，Logistic回归评估了前一夜TST和SE是否预测了回归。结果16例（27.6%）患者康复。较短的前夜TST与较高的逆转几率相关，而SE则无显著关联。随机夜间或长期睡眠测量显示没有关联。急性睡眠中断可能会短暂地损害认知并导致MCI错误分类。测试前的睡眠筛查可以提高诊断的可靠性。认知测试前一晚较短的总睡眠时间与1年后轻度认知障碍（MCI）恢复的几率较高相关。睡眠效率、随机夜间睡眠和14天平均睡眠与轻度认知障碍的恢复无显著关联。单域MCI病例比多域MCI病例更容易恢复，这表明对睡眠不足等急性因素的易感性更高。在MCI研究中，对前一晚睡眠或活动描记仪衍生指标进行简短筛选有助于识别低可靠性评估并提高诊断稳定性。
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