Alzheimer's & Dementia最新文献

{"title":"Blood transcriptomic signatures of vascular risk in Alzheimer's disease.","authors":"Sang-Won Han, Young Ho Park, Jung-Min Pyun, Jiyun Hwang, Jeong Su Park, SangYun Kim, Kwangsik Nho","doi":"10.1002/alz.71930","DOIUrl":"https://doi.org/10.1002/alz.71930","url":null,"abstract":"<p><strong>Introduction: </strong>Lifestyle and environmental factors contributing to cardiovascular risk are components of the exposome, yet molecular signatures associated with cumulative cardiovascular risk in Alzheimer's disease (AD) remain incompletely understood.</p><p><strong>Methods: </strong>We analyzed blood-based transcriptomics data from two independent cohorts: Seoul National University Bundang Hospital (SNUBH; N = 148, Korean) and Alzheimer's Disease Neuroimaging Initiative (ADNI; N = 743, predominantly European ancestry). Framingham cardiovascular risk score (FRS)-associated co-expression network modules were identified, followed by pathway-based enrichment, hub gene-based participant stratification, and bidirectional cross-cohort discovery-replication analyses.</p><p><strong>Results: </strong>Two co-expression modules were associated with FRS in SNUBH, and six in ADNI. Bidirectional analyses identified two preserved modules with consistent module-FRS associations across cohorts, enriched in pathways implicated in cellular responses to exposure, including RNA-protein homeostasis, mitochondrial function, and hematopoietic processes. Hub genes in the two modules stratified participants into molecularly distinct subgroups concordant with clinical FRS categories.</p><p><strong>Discussion: </strong>FRS-associated molecular pathways were identified and warrant further investigation as potential targets for risk modification.</p>","PeriodicalId":7471,"journal":{"name":"Alzheimer's & Dementia","volume":"22 10","pages":""},"PeriodicalIF":12.8,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149260413","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"UK Dementia Trials Network: an expert-informed framework for improving representation in dementia trials.","authors":"Igor C Fontana, Tara Comber, Sheena Aurora, Daniel J Blackburn, Rachel F Buckley, Christine Chow, Tiffany W Chow, Ruth Croney, Sebastian J Crutch, Karen Chilcott Holdridge, Lynne Hughes, Christopher Kipps, Susan Kohlhaas, Jorge Llibre-Guerra, Paresh Malhotra, Charles R Marshall, Stella McCaughey, Richard James Oakley, Rema Raman, Daniel Ridley, Shardae Showell, Richard Tsai, Catherine J Mummery","doi":"10.1002/alz.71928","DOIUrl":"https://doi.org/10.1002/alz.71928","url":null,"abstract":"<p><p>Alzheimer's disease (AD) is the leading cause of dementia worldwide, yet clinical trials remain unrepresentative of those most affected. Ethnic minoritized groups, socioeconomically deprived communities, adults over 75, and populations in low- and middle-income countries are consistently underrepresented, limiting generalizability and reinforcing health inequities. This white paper draws on an international roundtable on Diversity and Inclusion in Dementia Trials, convened by the UK Dementia Trials Network at the Alzheimer's Association International Conference 2025. We determined that key barriers to research participation included geographic distance, financial burden, restrictive eligibility criteria, invasive procedures, and limited study partner support. We also highlight gaps in ethnic diversity and the inadequate integration of sex and gender considerations in trial design and reporting. Improving representation in AD trials is both a scientific and moral imperative. Achieving this requires coordinated action across community engagement and trust building, data transparency and reporting, global trial access and capacity building, eligibility criteria reform, and financial and logistical support for participants. We propose an expert-informed implementation framework derived from the roundtable that identifies actionable strategies, responsible stakeholders, measurable indicators, and expected implementation outcomes to support translation of our recommendations into practice.</p>","PeriodicalId":7471,"journal":{"name":"Alzheimer's & Dementia","volume":"22 10","pages":""},"PeriodicalIF":12.8,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149260431","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pathway-specific polygenic risk scores modify the association between amyloid and tau PET accumulation in patients with Alzheimer's disease.","authors":"Carolina Valentim, Jannis Denecke, Simon Frerich, Tobey J Betthauser, Yuanxi Li, Reihaneh Ahmadi, Nicolai Franzmeier, Rainer Malik, Michael Ewers","doi":"10.1002/alz.71939","DOIUrl":"https://doi.org/10.1002/alz.71939","url":null,"abstract":"<p><strong>Background: </strong>Genome-wide association studies (GWASs) identified multiple genetic variants associated with Alzheimer's disease (AD) risk, yet the biological pathways linking these to amyloid and tau pathology remain unclear.</p><p><strong>Methods: </strong>We conducted a meta-analysis of recent GWASs to identify independent genome-wide significant single nucleotide polymorphisms which were mapped via gene-set enrichment to derive pathway-specific polygenic risk scores (pPRSs). Analyses included 441 amyloid-positive participants from the Alzheimer's Disease Neuroimaging Initiative (ADNI; 224 with longitudinal tau positron emission tomography [PET]) and 250 amyloid-positive participants from the Anti-Amyloid Treatment in Asymptomatic Alzheimer's Disease (A4) study (113 with longitudinal tau PET). Robust linear regressions tested cross-sectional and longitudinal pPRS-by-amyloid chronicity interactions on tau PET.</p><p><strong>Results: </strong>Four pPRSs were identified including adaptive immune response, leukocyte activation, transport, and intracellular signaling. Only the transport pPRS strengthened amyloid-tau coupling cross-sectionally across all Braak stages in ADNI (p < 0.05) and at Braak I in A4 (p < 0.05), with stronger effects observed in females; in ADNI, these associations persisted longitudinally only at the higher Braak stages.</p><p><strong>Discussion: </strong>Genetic variation in transport pathways modulates amyloid-driven tau accumulation, revealing mechanisms shaping AD progression, beyond apolipoprotein E.</p>","PeriodicalId":7471,"journal":{"name":"Alzheimer's & Dementia","volume":"22 10","pages":""},"PeriodicalIF":12.8,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149260379","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Real-world clinical, biomarker, and imaging outcomes of lecanemab in Alzheimer's disease: a multicenter longitudinal cohort study in Jiangsu, China.","authors":"Limoran Tang, Xicheng Chen, Li Zhang, Lin Fan, Nihong Chen, Chaosheng Li, Zenglin Cai, Guofang Chen, Haifeng Chen, Min Ye, Huifen Zheng, Qi Li, Zhihong Ke, Zheqi Hu, Maohong Cao, Dan Yang, Shuai Xu, Chunming Xie, Xiaobo Li, Xiaotian Xu, Ming Yu, Xuegan Lian, Hua Hu, Hongfei Li, Xiuying Cai, Hong Chen, Wu Xu, Guiyun Cui, Yang Zhao, Jingde Dong, Lili Zhang, Xiaolei Zhu, Hui Zhao, Yun Xu","doi":"10.1002/alz.71936","DOIUrl":"https://doi.org/10.1002/alz.71936","url":null,"abstract":"<p><strong>Introduction: </strong>Real-world data on lecanemab's efficacy and the longitudinal dynamics of plasma biomarkers are scarce in Chinese patients with Alzheimer's disease (AD).</p><p><strong>Methods: </strong>In this multicenter cohort study, 181 AD patients received biweekly lecanemab. Disease-stage-specific Clinical Dementia Rating-Sum of Boxes meaningful within-patient change defined response at Months 3, 6, and 12. We used penalized models, receiver operating characteristic analysis, attrition comparisons, and exploratory Month 3 plasma biomarker analysis.</p><p><strong>Results: </strong>Cognitive response emerged at Month 6 and intensified by Month 12, largely restricted to mild cognitive impairment and mild dementia due to AD. Repeated five-fold cross-validated areas under the curve across the follow-up timepoints were 0.560, 0.747, and 0.773, with apolipoprotein E ε4 positivity and more severe cognitive impairment linked to lower response odds. Plasma phosphorylated tau 217 (p-tau217) and amyloid beta (Aβ) 42/40 altered as early as Month 3. Month 3 Aβ42/40 showed modest exploratory discrimination. The incidence of amyloid-related imaging abnormalities was 7.2%, all asymptomatic.</p><p><strong>Discussion: </strong>Lecanemab is effective and safe in AD over 6 to 12 months. Early biomarker changes (p-tau217, Aβ42/40) precede clinical improvement, serving as scalable response indicators.</p>","PeriodicalId":7471,"journal":{"name":"Alzheimer's & Dementia","volume":"22 10","pages":""},"PeriodicalIF":12.8,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149260409","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The effects of improved access to diabetes medications on risk of Alzheimer's disease and related dementias.","authors":"Douglas Barthold, Julie Zissimopoulos, Anirban Basu, Bryan Tysinger","doi":"10.1002/alz.71794","DOIUrl":"10.1002/alz.71794","url":null,"abstract":"<p><strong>Introduction: </strong>Diabetes is associated with elevated risk of Alzheimer's disease and related dementias (ADRD). Disease management with pharmaceutical therapies may mitigate this increased risk, but access and use of diabetes therapies are limited, especially for persons at highest risk of ADRD.</p><p><strong>Methods: </strong>Using 10 years of data on Americans aged 51 and older with diabetes, we employed dynamic microsimulation to analyze the impact of increased utilization of glucagon-like peptide 1 receptor agonists (GLP1s) and sodium-glucose cotransporter-2 inhibitors (SGLT2s) on ADRD incidence.</p><p><strong>Results: </strong>Over 10 years, utilization of GLP1s and SGLT2s by people with diabetes and HbA1c > 7 could avert 76,000-201,000 ADRD cases. The risk reduction is largest for Black and Hispanic individuals and individuals with HbA1c > 8.</p><p><strong>Discussion: </strong>This study shows that improving diabetes management can lead to large reductions in ADRD risk. Improved adherence and access for those with higher HbA1c and higher risk of ADRD will have the largest benefit.</p>","PeriodicalId":7471,"journal":{"name":"Alzheimer's & Dementia","volume":"22 10","pages":"e71794"},"PeriodicalIF":12.8,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13655229/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149164401","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}

{"title":"Correction to Alzheimer's & dementia articles.","authors":"","doi":"10.1002/alz.71906","DOIUrl":"https://doi.org/10.1002/alz.71906","url":null,"abstract":"","PeriodicalId":7471,"journal":{"name":"Alzheimer's & Dementia","volume":"22 10","pages":""},"PeriodicalIF":12.8,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149260388","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Why sleep assessment belongs in the memory clinic.","authors":"Anastasia Suraev, Mariana Fernandes, Andrew Lim, Fang Han, Sharon L Naismith, Claudio Liguori","doi":"10.1002/alz.71880","DOIUrl":"https://doi.org/10.1002/alz.71880","url":null,"abstract":"<p><p>Sleep disturbances are highly prevalent in older adults and are particularly common among individuals attending memory clinics for assessment of cognitive impairment. Emerging evidence links sleep disorders, including insomnia, obstructive sleep apnea, circadian rhythm disruption, and rapid eye movement sleep behavior disorder, to cognitive decline, neurodegenerative pathology, and reduced quality of life for patients and caregivers. Despite their high prevalence and clinical relevance, sleep disturbances are not routinely assessed within many memory clinic and neurologic, psychiatric, and geriatric settings, and approaches to screening, diagnosis, and management vary widely across health-care systems. This Perspective article examines current approaches to sleep assessment and management within memory clinic and specialized settings across four international contexts. We highlight the absence of systematic approaches to identifying and managing sleep disturbances in this population and propose the need for a pragmatic stepped-care framework to improve detection, guide referral pathways, and support more consistent and personalized care in memory clinic settings.</p>","PeriodicalId":7471,"journal":{"name":"Alzheimer's & Dementia","volume":"22 10","pages":""},"PeriodicalIF":12.8,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149260452","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Excitation–inhibition imbalance links amyloid pathophysiology to cognition in non-demented individuals","authors":"Shaoshi Zhang,&nbsp;Sebastian N. Roemer-Cassiano,&nbsp;Joyce Ruifen Chong,&nbsp;Tian Fang,&nbsp;Yan Li,&nbsp;Ziwen Wang,&nbsp;Tianchu Zeng,&nbsp;Xin Li,&nbsp;Gustavo Deco,&nbsp;Narayanaswamy Venketasubramanian,&nbsp;Juan Helen Zhou,&nbsp;Christopher Li-Hsian Chen,&nbsp;Alzheimer's Disease Neuroimaging Initiative,&nbsp;Mitchell K. P. Lai,&nbsp;Nicolai Franzmeier,&nbsp;B. T. Thomas Yeo","doi":"10.1002/alz.71891","DOIUrl":"10.1002/alz.71891","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> INTRODUCTION</h3>\u0000 \u0000 <p>Excitation–inhibition (E/I) imbalance has been proposed as an early circuit-level mechanism in Alzheimer's disease (AD), but its relationship to molecular pathology and cognition in humans remains unclear.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> METHODS</h3>\u0000 \u0000 <p>We integrated biophysical modeling of resting-state functional magnetic resonance imaging with cerebrospinal fluid (CSF) and plasma biomarkers to examine whether E/I ratio links amyloid pathophysiology to memory in non-demented individuals across two cohorts from North America (<i>N</i> = 302; CSF amyloid beta 42 [Aβ42]) and Singapore (<i>N</i> = 240; plasma phosphorylated tau 217 [p-tau217]).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> RESULTS</h3>\u0000 \u0000 <p>Elevated E/I ratio was associated with lower CSF Aβ42 and higher plasma p-tau217, with greater sensitivity in sensory–motor regions. In contrast, elevated E/I ratio in association cortices was more strongly related to worse memory function. Mediation analyses indicated E/I ratio partially accounted for the AD biomarker–memory relationship.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> DISCUSSION</h3>\u0000 \u0000 <p>E/I imbalance represents an intermediate, systems-level circuit mechanism that links AD pathophysiology to cognitive impairment, offering novel insight into early neurophysiological changes along the AD continuum.</p>\u0000 </section>\u0000 </div>","PeriodicalId":7471,"journal":{"name":"Alzheimer's & Dementia","volume":"22 10","pages":""},"PeriodicalIF":12.8,"publicationDate":"2026-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13624711/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149079418","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}

{"title":"Associations of plasma HDL subclasses with incident dementia risk in older adults","authors":"Binchong An,&nbsp;Suad Ali,&nbsp;Karen Smith,&nbsp;Samantha Roemhild,&nbsp;Lindsey Neumann,&nbsp;Dwight R. Stoll,&nbsp;Ling Li,&nbsp;Pamela L Lutsey,&nbsp;Michelle M Mielke,&nbsp;Fang Yu,&nbsp;Ron C Hoogeveen,&nbsp;Lin Zhang,&nbsp;Alvaro Alonso,&nbsp;Danni Li","doi":"10.1002/alz.71893","DOIUrl":"10.1002/alz.71893","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> INTRODUCTION</h3>\u0000 \u0000 <p>Plasma high-density lipoprotein (HDL) varies in size. We examined the associations between HDL subclasses and their lipid composition and incident dementia risk in older adults.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> METHODS</h3>\u0000 \u0000 <p>We included 23,790 United Kingdom (UK) Biobank (UKB) and 147 Atherosclerosis Risk in Communities (ARIC) older adults free of dementia at baseline. HDL subclasses and their lipid composition were characterized using two distinct approaches: Nightingale nuclear magnetic resonance (NMR) spectroscopy in UKB and anion-exchange chromatography followed by mass spectrometry-based lipidomics of physically isolated HDL subfractions (AEX-MS) in ARIC. Cox regression models were used to evaluate the associations, adjusting for covariates.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> RESULTS</h3>\u0000 \u0000 <p>In the UKB, Nightingale NMR-derived plasma small and very large HDL particle and six lipid concentrations (total lipids, triglycerides [TG], phospholipids, free cholesterol, cholesterol ester [CE], total cholesterol) were associated with lower and higher risks of incident dementia, respectively. These associations were likely driven mainly by particle concentration in NMR-derived small HDL and by both lipid and lipid concentrations in NMR-derived very large HDL. In the ARIC, total TG in AEX-defined HDL subfraction 1 (e.g., smaller HDL), total lysophosphatidylcholine (LPC) and phosphatidylethanolamine (PE), and TG in AEX-defined subfraction 2 (e.g., larger HDL) were associated with a lower incident dementia risk.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> DISCUSSION</h3>\u0000 \u0000 <p>Although different HDL subclass characterization and lipid measurement methods made it difficult to compare results across cohorts, HDL subclasses and their lipid compositions were associated with the risk of incident dementia in both cohorts.</p>\u0000 </section>\u0000 </div>","PeriodicalId":7471,"journal":{"name":"Alzheimer's & Dementia","volume":"22 10","pages":""},"PeriodicalIF":12.8,"publicationDate":"2026-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/alz.71893","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149086016","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}

{"title":"ZBP1-mediated Treg cell dysfunction exacerbates neuroimmune dysregulation in Alzheimer's disease under metabolic stress","authors":"Shanshan Huang,&nbsp;Zengyu Zhang,&nbsp;Jiajie Xia,&nbsp;Mengqiu Deng,&nbsp;Fangzheng Chen,&nbsp;Meng Wang,&nbsp;Yuchao Fei,&nbsp;Zhiwen Jiang,&nbsp;Chenyu Lu,&nbsp;Jiayu Fu,&nbsp;Jingchun Guo,&nbsp;Houguang Zhou","doi":"10.1002/alz.71896","DOIUrl":"10.1002/alz.71896","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> INTRODUCTION</h3>\u0000 \u0000 <p>Metabolic stress increases Alzheimer's disease (AD) risk, but mechanisms linking metabolic dysfunction to neuroimmune dysregulation remain unclear.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> METHODS</h3>\u0000 \u0000 <p>We assessed cognition in community-dwelling participants and used high-fat diet (HFD)-fed 5xFAD mice, high glucose and high palmitate (HGHP)-treated regulatory T cell (Treg) co-cultures, and adoptive Treg transfer to evaluate metabolic stress-associated neuroimmune dysfunction. Flow cytometry, RNA sequencing, positron emission tomography computed tomography, and electrophysiology assessed Treg function, AD pathology, cerebral metabolism, and synaptic plasticity.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> RESULTS</h3>\u0000 \u0000 <p>Metabolic stress impaired Treg stability and function, accompanied by increased Z-DNA-binding protein 1 (ZBP1) expression and activation of apoptotic and necroptotic signaling. Treg dysfunction was associated with enhanced glial activation and neuronal injury. Under HGHP stress, ZBP1-deficient Tregs showed improved survival and stronger immunosuppressive activity, more effectively limiting glial activation and preserving neuronal integrity. In vivo, ZBP1-deficient Treg transfer conferred greater neuroprotection than wild-type Treg transfer in HFD-fed AD mice.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> DISCUSSION</h3>\u0000 \u0000 <p>ZBP1 may contribute to metabolic stress–induced Treg dysfunction and represent a candidate target to improve Treg-based therapy in HFD-fed AD mice.</p>\u0000 </section>\u0000 </div>","PeriodicalId":7471,"journal":{"name":"Alzheimer's & Dementia","volume":"22 10","pages":""},"PeriodicalIF":12.8,"publicationDate":"2026-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/alz.71896","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149086015","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}