Alzheimer's Research & Therapy最新文献

{"title":"Proteomic analysis in Alzheimer's disease and other dementias: a focus on sex-specific differences.","authors":"Aina Comas-Albertí, Albert Lladó, Diana Esteller-Gauxax, Sergi Borrego-Écija, Neus Falgàs, Farida Dakterzada, Agnès Pérez-Millan, Roger Puey, Tània Collet-Romà, Núria Guillén, Miquel Massons, Adrià Tort-Merino, Josep Maria Augé, Guadalupe Fernandez-Villullas, Bea Bosch, Raquel Ruiz-García, Laura Naranjo, Mircea Balasa, Gerard Piñol-Ripoll, Anna Antonell, Raquel Sánchez-Valle","doi":"10.1186/s13195-026-02068-7","DOIUrl":"https://doi.org/10.1186/s13195-026-02068-7","url":null,"abstract":"<p><strong>Background: </strong>Fluid protein studies in cerebrospinal fluid (CSF) and plasma have provided important insights into neurodegenerative dementias; however, there is a limited investigation of sex-related differences and cross-biofluid relationships. In Alzheimer's disease (AD), Lewy body dementia (LBD), and frontotemporal dementia (FTD), large-scale, sex-stratified analyses of paired CSF and plasma samples remain scarce. Using the multiplex and ultrasensitive capabilities of NULISAseq™ technology, this study aims to characterize sex- and disease-specific proteomic alterations associated with Central Nervous System (CNS) pathology to explore underlying mechanisms.</p><p><strong>Methods: </strong>CSF and plasma samples from 359 individuals with AD, LBD, FTD, and cognitively healthy controls were analyzed using the NULISAseq™ CNS Disease Panel 120. Differential protein expression analyses were conducted across diagnoses and stratified by sex, adjusting for relevant covariates. Spearman's correlation analyses were performed to assess concordance between CSF and plasma protein levels. All statistical analyses were conducted in R v4.4.3.</p><p><strong>Results: </strong>Differential protein expression analyses across diagnoses revealed two potential transdiagnostic biomarkers: ICAM1 in CSF and ANXA5 in plasma, showing consistent increases across AD, LBD, and FTD. Sex-stratified analyses in CSF showed modest changes, including higher CCL26, ANXA5, and IL10 in females with AD, and higher IL9, PRDX6, and CX3CL1 in males with AD. In LBD, females exhibited upregulation of ACHE, SFRP1, POSTN in both CSF and plasma. NPTX1 was identified as a potential CSF biomarker for FTD, showing downregulation particularly in males. In contrast, analyses stratified by sex in plasma displayed a larger number of proteins across all dementias, with females showing a higher number of upregulated inflammation-related proteins predominantly involved in cytokine signaling. Overall cross-fluid correlations were restricted to a small subset of proteins, indicating compartment-specific regulation.</p><p><strong>Conclusions: </strong>This study represents a large-scale, sex-stratified proteomic analysis of CSF and plasma across major neurodegenerative dementias using NULISAseq™ technology. The findings highlight sex-dependent biomarker patterns, particularly in plasma, and underscore the importance of incorporating sex as a biological variable in dementia research. Future studies should validate candidate proteins in independent cohorts, investigate their functional and mechanistic roles, and assess their utility for biomarker development and sex-tailored therapeutic strategies.</p>","PeriodicalId":7516,"journal":{"name":"Alzheimer's Research & Therapy","volume":" ","pages":""},"PeriodicalIF":7.6,"publicationDate":"2026-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147855745","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":"Income dynamics and risk of early-onset dementia: a nationwide cohort study.","authors":"Byung-Joon Ko, Yong-Moon Mark Park, Kyu-Na Lee, Kyungdo Han, Ga Eun Nam","doi":"10.1186/s13195-026-02067-8","DOIUrl":"https://doi.org/10.1186/s13195-026-02067-8","url":null,"abstract":"<p><strong>Background: </strong>The relationship between income dynamics-including sustained income level, income changes, and income variability-and early-onset dementia (EOD) has not been well established. This study investigated the association between income dynamics and the risk of EOD.</p><p><strong>Methods: </strong>This cohort study included 2,247,461 adults aged 40-60 years who underwent health examinations in 2012 through the Korean National Health Insurance Service, with a median follow-up duration of 5.4 years till 2018. Income status was assessed for 2012 and the 4 preceding years using monthly health insurance premiums, and income-related parameters were derived from this pre-baseline 5-year window. Income variability was defined as the intra-individual standard deviation of four consecutive annual percentage changes. Hazard ratios (HRs) and 95% confidence intervals (CIs) were estimated to evaluate the relationship between income dynamics and EOD risk, adjusting for potential confounders.</p><p><strong>Results: </strong>Sustained low-income status over five years was associated with an increased risk of EOD (HR for 5 years vs. 0 years 1.63, 95% CI 1.49-1.78; P-trend < 0.001), whereas sustained high-income status was associated with a reduced EOD risk (HR for 5 years vs. 0 years 0.55, 95% CI 0.51-0.59; P-trend < 0.001). Notably, higher income variability was linked to a greater risk of EOD (HR for highest vs. lowest quartile 1.37, 95% CI 1.28-1.48; P-trend < 0.001). The decline in income-particularly to the lowest level (Medical Aid beneficiaries)-was associated with an elevated risk of EOD, irrespective of the initial income status.</p><p><strong>Conclusions: </strong>Sustained low income, income decline, and greater income variability were associated with higher EOD risk. These findings may help identify socioeconomically vulnerable middle-aged adults for targeted dementia risk assessment and prevention.</p>","PeriodicalId":7516,"journal":{"name":"Alzheimer's Research & Therapy","volume":" ","pages":""},"PeriodicalIF":7.6,"publicationDate":"2026-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147855639","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":"Early syndecan-4 upregulation predicts cognitive and pathological trajectories in Alzheimer disease.","authors":"Rawan Tarawneh, Krista L Moulder, Danai G Topouza, Amrita Kar, Heng Tony Qian, Vernon S Pankratz, Jigyasha Timsina, Erin E Franklin, Suzanne E Schindler, Richard J Perrin, Beau M Ances, Tammie L S Benzinger, Jason Hassenstab, John C Morris, David M Holtzman, Carlos Cruchaga","doi":"10.1186/s13195-026-02043-2","DOIUrl":"https://doi.org/10.1186/s13195-026-02043-2","url":null,"abstract":"<p><strong>Background: </strong>Brain endothelial dysfunction is an early pathological feature of Alzheimer disease (AD). We here investigate associations of the brain endothelial glycocalyx protein, syndecan-4 (SDC4), with amyloid and tau pathologies and cognitive impairment in a large longitudinal cohort of AD and controls.</p><p><strong>Methods: </strong>The study included n = 1,041 (n = 802 cognitively unimpaired and n = 239 cognitively impaired) participants who underwent biological classification using the NIA-AA \"ATN\" framework. Cognitive assessments included the Clinical Dementia Rating^®-sum of boxes and the Knight- Preclinical Alzheimer's Cognitive Composite. Cerebrospinal fluid (CSF) measures of SDC4 and emerging AD biomarkers were obtained using Olink Proteomics. Amyloid-PET (n = 719) and tau-PET (n = 302) scans were performed in subsets of participants. Partial correlations and linear mixed models, respectively, examined cross-sectional and longitudinal associations of CSF SDC4 levels with amyloid-PET and tau-PET burden and cognition. Pseudo-time models estimated CSF biomarker trajectories across the course of AD progression.</p><p><strong>Results: </strong>CSF SDC4 levels were elevated in even the earliest preclinical stages of AD compared to controls and were closely associated with other CSF and imaging biomarkers of AD. Higher CSF SDC4 levels correlated with higher global and regional amyloid-PET and tau-PET burden and worse baseline cognition. Higher baseline CSF SDC4 levels predicted more rapid progression of brain amyloid and tau, and faster decline in global cognition, episodic memory, language, and executive functions over follow-up (mean, 8 years). CSF SDC4 associations with cognition were mainly mediated by global tau-PET burden. Importantly, our pseudo-time models estimate that SDC4 upregulation begins very early in AD pathogenesis near the point of amyloid-positivity and increases more robustly following the point of tau-positivity. SDC4 was among the top 10 most important proteins in predicting the pseudo-time models of AD progression and predicted these models to a potentially better extent than other emerging AD biomarkers.</p><p><strong>Conclusion: </strong>Findings from this large longitudinal study suggest that CSF SDC4 levels are increased in the earliest preclinical stages of AD and are closely associated with the progression of amyloid and tau pathologies and future rates of cognitive decline. We propose that SDC4 upregulation is an important early event in AD pathogenesis which predicts cognitive and pathological disease trajectories.</p>","PeriodicalId":7516,"journal":{"name":"Alzheimer's Research & Therapy","volume":" ","pages":""},"PeriodicalIF":7.6,"publicationDate":"2026-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147832253","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":"Impact of Apolipoprotein E4 on blood-brain barrier integrity in target replacement murine models: a systematic review and meta-analysis.","authors":"Krystal K Laing, Nela Fialova, Joanna Wardlaw, Axel Montagne","doi":"10.1186/s13195-026-02018-3","DOIUrl":"https://doi.org/10.1186/s13195-026-02018-3","url":null,"abstract":"<p><strong>Background: </strong>The E4 variant of Apolipoprotein E (APOE) is a primary genetic susceptibility risk factor for late-onset Alzheimer's disease and has been implicated in cerebrovascular dysfunction. Preclinical mouse models are widely used to study APOE4, but cohesive understanding of APOE's role is still inconsistent and lacking. The aim of this study was to systematically review and synthesise evidence from preclinical mouse studies assessing APOE4 related effects on blood-brain barrier (BBB) integrity, vascular morphology and cerebral blood flow (CBF). MAIN: A systematic search of MEDLINE, Embase, Scopus, and Web of Science was conducted (March-April 2025). Eligible studies included transgenic APOE-targeted replacement or knock-in mice reporting vascular outcomes (cerebral blood flow, blood brain barrier permeability, vascular measures). Risk of bias was assessed using SYRCLE and reporting quality with CAMARADES. Random-effects meta-analyses were conducted (where sufficient data was available), otherwise findings were narratively synthesised. Eighteen studies met inclusion. Outcome measures varied widely, including diverse approaches to CBF measurement (e.g. arterial spin labelling, autoradiography, DSC-MRI), immunohistochemical measures (e.g. collagen-IV, laminin, CD31), and diverse approaches to measurement of BBB leakage (e.g. fibronectin, fibrinogen, gadolinium-based ktrans). Seven studies contributed to meta-analysis: APOE4 mice showed a consistent reduction in CBF associated with APOE4 genotype (SMD = -2.87, 95% CI: -5.14 to -0.604, df = 2.66), and a negative non-significant trend towards reduced vascular morphology expression. Narrative synthesis identified three key mechanistic pathways linking APOE4 to vascular dysfunction: (i) insulin resistance and PI3K/AKT-mTOR signalling, (ii) Cyclophilin A-NFκB-MMP9 activation, and (iii) occludin/ECM remodelling. Risk of bias assessment revealed frequent shortcomings in randomisation, blinding, and sample size justification.</p><p><strong>Conclusions: </strong>Preclinical evidence demonstrates that APOE4 drives alterations in vascular functioning primarily through involvement with pathways related to vascular metabolism, ECM remodelling and BBB leakage. However, heterogeneity in the model (e.g. age, sex, techniques), restricts direct comparability across studies. As such, standardisation or clarification of methodological approaches are necessary for rigorous assessment in the future.</p>","PeriodicalId":7516,"journal":{"name":"Alzheimer's Research & Therapy","volume":" ","pages":""},"PeriodicalIF":7.6,"publicationDate":"2026-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147832284","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":"Aging alters the vulnerability pattern to amyloid-beta oligomers in wild-type mice: a behavioral and neurobiological study.","authors":"Ahmad Allouche, Julie Colin, Catherine Birck, Henri Schroeder, Valentin Tallandier, Marion Baldoni, Christophe Muller, Mohamed Afrassi, Nicolas Violle","doi":"10.1186/s13195-026-02051-2","DOIUrl":"https://doi.org/10.1186/s13195-026-02051-2","url":null,"abstract":"<p><strong>Background: </strong>Aging is the primary risk factor for sporadic Alzheimer's disease (AD). While amyloid-beta oligomers (AβOs) accumulation is a key neuropathological process in AD, their specific effects in aged brains and how aging modulates brain response to AβOs remains poorly understood. We investigated how aging contributes to AβO-induced neurotoxicity and cognitive deficits in mice.</p><p><strong>Methods: </strong>After biochemical and in vitro characterizations on primary cultures of cortical neurons, AβOs or their vehicle were intracerebrally injected into both 3- and 18-month-old wild-type mice. A broad spectrum of assays including synaptic markers, neuroinflammation, apoptosis and cognitive functions was used to establish a preliminary characterization of the interplay between age and AβOs. In vivo data were analyzed using a multifactorial design (Treatment × Age), with two-way ANOVA or other appropriate statistical models.</p><p><strong>Results: </strong>Old mice had significantly reduced synaptic proteins SNAP-25 and PSD-95, elevated neuroinflammatory markers, and increased neuronal apoptosis in hippocampus and cortex, despite showing cognitive performances similar to young mice. All brain biomarkers were worsened after AβO injection in both young and old mice. Age and AβO effects either accumulated or interacted to promote neuroinflammation and apoptosis, depending on brain areas, whereas their effects on synaptic proteins were strictly additive. Moreover, AβO injection induced only mild spatial memory deficits in young mice, in contrast with those observed in old mice in both episodic and spatial memory tests.</p><p><strong>Discussion: </strong>Whereas the young brain showed resilience to maintain memory performances after AβO injection, the coping capacities of the aging brain were exceeded by AβO effects. At the neurobiological level, age and AβO effects were mainly additive, but also acted synergistically in a brain region-dependent vulnerability pattern. This study highlights the value of incorporating aging into preclinical models to improve their translational validity and enhance their relevance for drug testing targeting early stages of sporadic AD.</p>","PeriodicalId":7516,"journal":{"name":"Alzheimer's Research & Therapy","volume":" ","pages":""},"PeriodicalIF":7.6,"publicationDate":"2026-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147809328","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":"Incidence of primary progressive aphasia in Salento, Italy: a population-based study.","authors":"Daniele Urso, Alessandra Vitulli, Stefano Giannoni-Luza, Valentina Gnoni, Alessia Giugno, Eleonora Rollo, Davide Vilella, Chiara Zecca, Nicolas Ray, Giancarlo Logroscino","doi":"10.1186/s13195-026-02046-z","DOIUrl":"https://doi.org/10.1186/s13195-026-02046-z","url":null,"abstract":"<p><strong>Introduction: </strong>Data on the population-based incidence of primary progressive aphasia (PPA), including all variants and Alzheimer's disease (AD) biomarker profiles, are scarce.</p><p><strong>Methods: </strong>We conducted a 4-year, prospective, population-based study in the Salento region of Southern Italy, identifying incident PPA cases through a territory-wide surveillance network. Clinical diagnoses followed consensus criteria; AD pathology was defined by positive CSF or amyloid PET biomarkers.</p><p><strong>Results: </strong>We identified 35 incident PPA cases, yielding an overall incidence of 1.14 (95% CI, 0.79-1.59) per 100,000 person-years. Incidence peaked in the early 60s for men and in the late 70s for women. The logopenic variant was most frequent and invariably associated with AD pathology. Approximately 20% of nonfluent and semantic cases, and the majority unclassified cases, also showed AD biomarkers.</p><p><strong>Discussion: </strong>These findings provide real-world epidemiological evidence and underscore the need for systematic biomarker assessment in PPA to guide diagnosis, prognosis, and access to emerging therapies.</p>","PeriodicalId":7516,"journal":{"name":"Alzheimer's Research & Therapy","volume":" ","pages":""},"PeriodicalIF":7.6,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147809357","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":"Cognitive Reserve in rural and urban populations: Insights from two aging cohorts in southern India.","authors":"Ramya Burra, Palash K Malo, Hitesh Pradhan, Raghav Prasad, Pooja Rai, Thomas G Issac, Jonas S Sundarakumar, Siva Athreya, Rajesh Sundaresan","doi":"10.1186/s13195-026-02031-6","DOIUrl":"https://doi.org/10.1186/s13195-026-02031-6","url":null,"abstract":"<p><strong>Background: </strong>There are no Indian studies estimating Cognitive Reserve (CR) across rural and urban aging populations.</p><p><strong>Methods: </strong>We estimated CR from two ongoing aging studies in rural (CBR-SANSCOG, n = 4459) and urban (CBR-TLSA, n = 663) southern India. We used years of education (YOE), job skill level (JSL), social network diversity (SND) and multilingualism (ML) as factors and assigned weights based on their capability to predict cognitive performance (assessed using a culturally adapted cognitive test battery). We evaluated several candidate machine learning models and chose the linear regression based on its fit.</p><p><strong>Findings: </strong>In the rural cohort, YOE, ML, and SND contributed significantly (Rural CR = 0.085×YOE + 0.184×ML + 0.030×SND), whereas YOE, ML and JSL were significant contributors for the urban cohort (Urban CR = 0.064×YOE + 0.184×ML + 0.197×JSL).</p><p><strong>Interpretation: </strong>The contribution of CR factors differs across rural and urban Indian populations. Targeted interventions to enhance population-specific CR factors could reduce dementia risk.</p>","PeriodicalId":7516,"journal":{"name":"Alzheimer's Research & Therapy","volume":" ","pages":""},"PeriodicalIF":7.6,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147809395","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":"Performance of plasma pTau217, pTau181 and their ratios to Aβ42 in detecting Aβ pathology using a China-developed direct chemiluminescence assay.","authors":"Dan Yang, Zhihong Ke, Nihong Chen, Ling Yue, Shuai Chen, Maoyuan Jiang, Zheqi Hu, Chunming Xie, Wenhao Zhu, Jingxian Xu, Linjie Yu, Limoran Tang, Hui Zhao, Jingde Dong, Chaosheng Li, Guofang Chen, Benyan Luo, Jiewen Zhang, Yun Xu","doi":"10.1186/s13195-026-02058-9","DOIUrl":"https://doi.org/10.1186/s13195-026-02058-9","url":null,"abstract":"<p><strong>Background: </strong>Increasing evidence indicates that blood-based biomarkers, particularly phosphorylated tau (pTau) 217 and the pTau217/amyloid‑β (Aβ) 42 ratio, demonstrate strong diagnostic performance for Alzheimer's disease (AD) and may offer a minimally invasive alternative to cerebrospinal fluid (CSF) assays and Aβ PET imaging. There is an urgent need to develop local plasma pTau217 and pTau217/Aβ42 ratio assay and to establish population-appropriate diagnostic cutoffs tailored to Chinese populations.</p><p><strong>Methods: </strong>This study included 831 individuals from a community-based memory screening cohort and 301 patients from a hospital-based cohort with confirmed Aβ pathology. Plasma pTau217, pTau181, and their ratios to Aβ42 were measured using a high-sensitivity direct chemiluminescence (DCL) immunoassay incorporating proprietary China-developed antibodies. Data-driven Gaussian mixture modeling (GMM) was applied to the community cohort to derive biomarker cutoffs; the diagnostic performance of these cutoffs was validated in the patients with confirmed Aβ pathology. A two-cutoff approach was established in the hospital-based cohort. Multivariate regression analysis was performed to assessed potential confounding effects from routine blood biochemical parameters.</p><p><strong>Results: </strong>GMM identified cutoffs of 4.380 pg/mL for pTau217 and 0.670 for the pTau217/Aβ42 ratio. These values closely matched cutoffs derived from the maximum Youden index (4.296 pg/mL for pTau217 and 0.706 for pTau217/Aβ42) and achieved high diagnostic accuracy (up to 89%) for Aβ pathology in the hospital-based cohort with confirmed Aβ pathology, outperforming pTau181-based measures. Only the pTau217/Aβ42 ratio was unaffected by routine plasma biochemistry. Using a two-cutoff workflow, pTau217 or the pTau217/Aβ42 ratio definitively classified approximately 90% of patients as positive or negative, leaving an intermediate-risk zone of < 10%.</p><p><strong>Conclusions: </strong>The China-developed DCL immunoassay reliably measures plasma pTau217 and the pTau217/Aβ42 ratio with high diagnostic accuracy for detecting Aβ pathology. The biochemical stability of the pTau217/Aβ42 ratio supports its potential as a practical, less invasive alternative to CSF or PET testing in Chinese populations.</p>","PeriodicalId":7516,"journal":{"name":"Alzheimer's Research & Therapy","volume":" ","pages":""},"PeriodicalIF":7.6,"publicationDate":"2026-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147759740","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":"Acetylcholinesterase inhibitors and the risk of delirium - a Danish nationwide register-based cohort study.","authors":"Martin Torp Rahbek, Helene Kildegaard, Jesper Hallas, Martin Thomsen Ernst, Lars Christian Lund","doi":"10.1186/s13195-026-02060-1","DOIUrl":"https://doi.org/10.1186/s13195-026-02060-1","url":null,"abstract":"","PeriodicalId":7516,"journal":{"name":"Alzheimer's Research & Therapy","volume":" ","pages":""},"PeriodicalIF":7.6,"publicationDate":"2026-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147759497","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":"Impact of appendicular skeletal muscle mass on Alzheimer's disease in relation to age and comorbidities: an 8-year longitudinal follow-up study of a nationwide cohort.","authors":"Su Jin Chung, Minwoong Kang, Yu Jeong Park, Kyungmi Oh, Seong-Beom Koh, Sung Hoon Kang","doi":"10.1186/s13195-026-02063-y","DOIUrl":"https://doi.org/10.1186/s13195-026-02063-y","url":null,"abstract":"","PeriodicalId":7516,"journal":{"name":"Alzheimer's Research & Therapy","volume":" ","pages":""},"PeriodicalIF":7.6,"publicationDate":"2026-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147759712","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}