Journal of Alzheimer's Disease最新文献

{"title":"Diluting the signal: Class-level pooling and the ecological fallacy in meta-analyses of anti-amyloid monoclonal antibodies.","authors":"Guilherme Riccioppo Rodrigues","doi":"10.1177/13872877261467048","DOIUrl":"10.1177/13872877261467048","url":null,"abstract":"<p><p>The recent Cochrane review of amyloid-β-targeting monoclonal antibodies concludes that future research on disease-modifying treatments for Alzheimer's disease should focus on alternative mechanisms. This conclusion rests on class-level pooling of nine pharmacologically heterogeneous agents, only three of which received FDA approval. This analytical decision commits an ecological fallacy at the drug level, diluting the signal of the agents that have modified clinical practice. This commentary situates the review within the broader literature, discusses the methodological origins of the error, and argues for stratified approaches that preserve clinical and regulatory relevance in syntheses of heterogeneous drug classes.</p>","PeriodicalId":14929,"journal":{"name":"Journal of Alzheimer's Disease","volume":" ","pages":"95-96"},"PeriodicalIF":3.4,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148390960","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Eligibility for lecanemab therapy in a biomarker defined memory clinic cohort: A five-year analysis.","authors":"Pablo Agüero-Rabes, Javier Roa-Escobar, Raquel Téllez, Verónica Mañanes, Estrella Gómez-Tortosa","doi":"10.1177/13872877261466695","DOIUrl":"10.1177/13872877261466695","url":null,"abstract":"<p><p>We assessed cross-sectional lecanemab eligibility (January 2026) in 479 patients with mild cognitive impairment or dementia who underwent Alzheimer's disease (AD) biomarker testing at a tertiary memory clinic (2021-2025). Overall eligibility was 16%, with exclusions due to negative biomarkers (41%), advanced disease stage (31%), <i>APOE</i> ε4/ε4 homozygosity (6%), and other safety reasons (6%). In the 2025 subgroup (n = 100), eligibility increased to 32%, reflecting fewer exclusions for disease progression and a targeted evaluation of patients likely to meet criteria. These findings highlight a narrow post-diagnosis therapeutic window and suggest an upper eligibility limit under the current appropriate use recommendations for anti-amyloid therapies.</p>","PeriodicalId":14929,"journal":{"name":"Journal of Alzheimer's Disease","volume":" ","pages":"89-94"},"PeriodicalIF":3.4,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148404736","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The association between retinal vascular occlusions and dementia using TriNetX.","authors":"Michelle A Spratt, Millen S Khangura, Ambika Manhapra, Audrey Gao, Nicole H Siegel, Vasiliki Poulaki, Steven Ness, Manju L Subramanian","doi":"10.1177/13872877261481012","DOIUrl":"https://doi.org/10.1177/13872877261481012","url":null,"abstract":"<p><p>BackgroundRetinal vascular occlusions have been associated with higher incidence of dementia and may serve as clinical indicators for underlying cognitive disease.ObjectiveThis study investigated whether retinal vascular occlusion and their subtypes are linked to increased risk of dementia, including all-cause dementia, Alzheimer's disease (AD), and vascular dementia (VaD).MethodsParticipants age 65 and over were categorized into eight groups using the TriNetX global database: 1) Retinal vascular occlusion, 2) Retinal artery occlusions (RAO), 3) Retinal vein occlusions (RVO), 4) Central retinal artery occlusions (CRAO), 5) Branch retinal artery occlusions (BRAO), 6) Central retinal vein occlusions (CRVO), 7) Branch retinal vein occlusions (BRVO), and 8) No retinal vascular occlusions. Groups were propensity score matched 1:1 for demographic and clinical covariates. Outcomes include the risk of all-cause dementia, AD, and VaD, assessed using Cox proportional hazard ratios with 95% confidence intervals. Kaplan-Meier analysis evaluated time to dementia onset.ResultsThe TriNetX database identified 21,367 individuals with retinal vascular occlusion who were followed for an average of 6.29 years. Participants with retinal vascular occlusions, RVOs, or BRVOs demonstrated higher risk of all-cause dementia and VaD. There were no increased associations for retinal vascular occlusions and AD.ConclusionsRetinal vascular occlusions and RVOs were associated with an increased risk of all-cause dementia and VaD, but not AD. No associations were found with RAOs. Retinal vein occlusions may serve as a potential clinical marker for underlying neurodegenerative disease and emphasize the need for careful monitoring in patients with retinal vascular occlusions.</p>","PeriodicalId":14929,"journal":{"name":"Journal of Alzheimer's Disease","volume":" ","pages":"13872877261481012"},"PeriodicalIF":3.4,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148873945","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mitophagy deficiency and calcium dyshomeostasis underlying the pathogenesis and progression of Alzheimer's disease.","authors":"Guangrong Meng, Liang Cai, Zhongcheng Mo, Shaoying An, Wenhui Sun, Ping Shen, Yuanjie Xie","doi":"10.1177/13872877261465779","DOIUrl":"10.1177/13872877261465779","url":null,"abstract":"<p><p>Alzheimer's disease (AD) is a neurodegenerative disorder defined by three pathological hallmarks: amyloid-β (Aβ) deposition, tau hyperphosphorylation leading to neurofibrillary tangles formation, and neuronal loss. Mounting evidence over the past decade has underscored that mitophagy deficiency and calcium dyshomeostasis play pivotal regulatory roles in AD pathological progression, with these two abnormalities persisting throughout the entire course of disease onset and development. Mitophagy impairment can result in the accumulation of dysfunctional mitochondria, thereby further exacerbating calcium dyshomeostasis which can suppress autophagic flux in turn. This reciprocal interaction establishes a vicious cycle that can synergistically accelerate Aβ plaque and neurofibrillary tangle formation, impair synaptic structure and function, and ultimately elicit neuronal programmed cell death and cognitive decline. This review systematically summarizes the biological basis of mitophagy and calcium homeostasis, as well as their mutual regulatory networks. It places particular emphasis on deciphering the pathological mechanisms through which concurrent impairments of these two pathways synergistically drive AD pathogenesis and progression. Furthermore, we propose intervention strategies targeting to modulate mitophagy deficiency and calcium dyshomeostasis, which hold great promise for providing novel insights and potential therapeutic targets for the clinical management of AD.</p>","PeriodicalId":14929,"journal":{"name":"Journal of Alzheimer's Disease","volume":" ","pages":"16-35"},"PeriodicalIF":3.4,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148421384","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Bilingualism and cognition: The impact of age of acquisition, language use, and proficiency in cognitively unimpaired older adults.","authors":"Sergio Grueso, Gonzalo Sánchez-Benavides, Miguel Santos-Santos, Laia Subirats, Ferran Prados, Oriol Grau-Rivera, Marco Calabria","doi":"10.1177/13872877261469525","DOIUrl":"10.1177/13872877261469525","url":null,"abstract":"<p><p>BackgroundThe positive effect of bilingualism as a cognitive reserve factor in aging remains inconclusive, with inconsistencies often stemming from treating bilingualism as a dichotomous variable rather than a dynamic, multidimensional experience.ObjectiveTo investigate the impact of bilingualism on cognition in cognitively unimpaired older adults, focusing on age of language acquisition (AoA), proficiency, and usage throughout life.MethodsData from 2415 participants (aged 45-74) from the Alzheimer's and Families (ALFA) study were analyzed. Cognitive assessments included the Mini-Mental State Examination to assess global cognition, semantic verbal fluency for semantic lexical retrieval, Memory Binding Test for verbal episodic memory, and WAIS-IV subtests for processing speed (Coding), visual-spatial reasoning (Visual Puzzles), non-verbal abstract reasoning (Matrix Reasoning), verbal short-term memory and attention (Digit Span Forward) and working memory (Digit Span Backward and Sequencing). We defined three groups based on AoA (Early/Late) and proficiency (High/Low) of Catalan: 1) Early High-Proficiency bilinguals (n = 1559); 2) Late High-Proficiency bilinguals (n = 537) and 3) Late Low-Proficiency bilinguals, primarily Spanish-dominant (n = 319).ResultsEarly and Late High-Proficiency bilingual groups outperformed Late Low-Proficiency bilinguals in verbal semantic fluency and processing speed. Additionally, Early High-Proficiency bilinguals scored significantly higher in verbal short-term memory than both Late AoA groups.ConclusionsThe effects of bilingualism are domain-specific and primarily driven by high proficiency and active language use rather than AoA alone. These findings suggest that maintaining high L2 proficiency throughout the lifespan contributes to cognitive reserve, enhancing attentional control and processing speed in healthy aging.</p>","PeriodicalId":14929,"journal":{"name":"Journal of Alzheimer's Disease","volume":" ","pages":"424-440"},"PeriodicalIF":3.4,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148470764","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Episodic memory and associated cortical atrophy in amnestic early-onset and late-onset Alzheimer's disease.","authors":"Cierra M Keith, Marc W Haut, Patrick Worhunsky, Camila Vieira Ligo Teixeira, Rashi I Mehta, Joseph Malone, Holly Phelps, Melanie Ward, Mark Miller, Stephanie Pockl, Nafiisah Rajabalee, Gary Marano, William T McCuddy, Pierre-François D'Haese, Ali Rezai","doi":"10.1177/13872877261469183","DOIUrl":"10.1177/13872877261469183","url":null,"abstract":"<p><p>BackgroundMemory consolidation problems are often prototypical in Alzheimer's disease (AD). However, it remains undetermined whether episodic memory presents similarly in early-onset Alzheimer's disease (EOAD) relative to the more commonly occurring late-onset Alzheimer's disease (LOAD).ObjectiveThis study examined episodic memory and its neuroanatomical correlates in amnestic early-onset (aEOAD) relative to amnestic late-onset AD (aLOAD).MethodsUsing our single center data set obtained from a memory clinic setting (N = 180), we examined group differences in multiple markers of episodic memory along with associations with volume and thickness of underlying signature brain regions.ResultsWe did not observe any difference for examined measures of memory performance between aEOAD and aLOAD. Associations between episodic memory processes and volume and thickness of the brain regions examined were also largely similar, except for a stronger relationship between memory consolidation and thinner left supramarginal gyrus observed in the aEOAD group.ConclusionsOverall, the current results support similar memory consolidation processes in early- and late-onset amnestic Alzheimer's disease, though the parietal cortex may play a larger role in memory consolidation in aEOAD.</p>","PeriodicalId":14929,"journal":{"name":"Journal of Alzheimer's Disease","volume":" ","pages":"403-413"},"PeriodicalIF":3.4,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13499921/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148562055","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Impact of SARS-CoV-2 infection on the progression of Alzheimer's disease: A prospective cohort study.","authors":"Jiating Qiu, Yishu Zhang, Yajun Shang, Qunzhu Shang, Lu Li, Yili Chen, Shujuan Dai, Mingda Ai, Xiaoting Xi, Wei Huang, Junyan Zhang, Xiaolei Liu","doi":"10.1177/13872877261469118","DOIUrl":"10.1177/13872877261469118","url":null,"abstract":"<p><p>BackgroundSARS-CoV-2 infection is associated with neurological sequelae and may accelerate Alzheimer's disease (AD) progression through neuroinflammation and protein aggregation. However, longitudinal evidence regarding the cognitive impact of COVID-19 in patients with AD remains scarce, and this interaction requires further clarification.ObjectiveTo explore whether COVID-19 accelerates cognitive decline in patients with AD.MethodsA total of 120 participants were enrolled, including 63 in the COVID-19 group and 57 in the non-COVID-19 group. The primary outcomes were disease decline and disease deterioration over three months, assessed using CDR-SB. Disease deterioration indicated clinically meaningful worsening, whereas disease decline captured subtler progression. Multivariable logistic regression adjusted for demographic, clinical, lifestyle, genetic, and disease severity factors. Overlap-Weighted Propensity Score Matching was additionally performed to reduce confounding during the 3-month follow-up.ResultsCOVID-19 significantly increased the risk of disease decline (OR = 10.39, 95% CI:3.87 to 27.87, p < 0.001) and disease deterioration (OR = 10.37, 95% CI: 2.71 to 39.65, p = 0.001). <i>APOE</i> ε4 carrier status was associated with a higher risk of deterioration (OR = 1.72), while those with unknown <i>APOE</i> status exhibited an even greater risk (OR = 5.20, 95% CI:1.32 to 20.53, p = 0.019). Secondary analyses confirmed that COVID-19 patients experienced significantly greater increases in CDR-SB scores compared to non-COVID-19 patients.ConclusionsSARS-CoV-2 infection was associated with greater short-term cognitive worsening over a three-month period in patients with AD, underscoring its potential public health relevance and the need for early surveillance to guide timely clinical management.</p>","PeriodicalId":14929,"journal":{"name":"Journal of Alzheimer's Disease","volume":" ","pages":"353-365"},"PeriodicalIF":3.4,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148678411","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Precuneus amyloid-β deposition involving the association of irritability and cognitive decline: A multi-cohort longitudinal study.","authors":"Yuanyuan Liu, Qi Qiu, Ling Yue, Bo Hong, Ning Su, Wei Li, Shifu Xiao, Lin Sun, Jianhua Chen","doi":"10.1177/13872877261467432","DOIUrl":"10.1177/13872877261467432","url":null,"abstract":"<p><p>BackgroundIrritability is increasingly recognized for its association with cognitive function, though its impact on cognitive decline and underlying mechanisms remain unclear.ObjectiveTo investigate the associations between irritability and cognition, identify potential neurobiological mechanisms.MethodsThis study included three cohorts: the Alzheimer's Disease Neuroimaging Initiative (ADNI, N = 722), the UK Biobank (UKB, N = 405,112), and the China Longitudinal Aging Study (CLAS, N = 240). Participants were classified into irritability-positive (+) and irritability-negative (-) groups based on assessment of irritability.We used Linear mixed-effects models to assess irritability-related cognitive trajectory, Cox regression to estimate cognitive decline, mediation analysis to test the effect of amyloid-β (Aβ) on the relationship between irritability and cognitive decline, and enrichment analysis to identify the underlying pathological mechanisms of irritability.ResultsIrritability was associated with increased cognitive decline in both ADNI (HR = 1.49, 95% CI: 1.12-1.98) and UKB (HR = 1.09, 95% CI: 1.04-1.15) cohorts, with baseline irritability linked to faster Mini-Mental State Examination decline (2.76 versus 1.88). Mediation analysis showed that cerebrospinal fluid (CSF) Aβ mediated 19-24% of irritability's effect on cognitive decline, while precuneus Aβ pathology mediated 30-41%. Imaging analysis revealed significant thinning of the left precuneus cortex in individuals with irritability. Proteomic analysis indicated underlying pathways involving enhanced energy metabolism and suppressed signal transduction, with modifiable factors (air pollution and physical inactivity) associated with irritability-related pathological proteins.ConclusionsOur findings indicate that irritability is significantly associated with cognitive decline. This association may be driven by mechanisms involving precuneus pathology, increased energy metabolism, and suppressed signal transduction, though these results warrant confirmation in future studies.</p>","PeriodicalId":14929,"journal":{"name":"Journal of Alzheimer's Disease","volume":" ","pages":"198-215"},"PeriodicalIF":3.4,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148562089","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Long-term locus coeruleus stimulation exacerbates tau pathology in PS19 mice.","authors":"Yuhan Nong, Steven Wellman, Hong Zhang, Yuxiang Andy Liu, Elentina K Argyrousi, Ottavio Arancio, Qi Wang","doi":"10.1177/13872877261468577","DOIUrl":"10.1177/13872877261468577","url":null,"abstract":"<p><p>BackgroundAlzheimer's disease (AD) is the most common form of dementia, characterized by the accumulation of amyloid-β (Aβ) plaques and hyperphosphorylated tau tangles. The locus coeruleus (LC) is among the first brain regions to show degeneration and tau pathology during the early stages of AD. Previous studies have demonstrated that short-term chemogenetic LC stimulation can improve memory performance in the TgF344-AD rat model, while long-term norepinephrine reuptake inhibition can worsen memory deficits in the ADLP^Tau mouse model. However, the effects of long-term LC stimulation in tau mouse models on memory, synaptic plasticity, and tauopathy remain unclear.ObjectiveTo evaluate the impact of long-term LC stimulation on memory, synaptic plasticity, and tauopathy in PS19 mice using behavioral paradigms, electrophysiological recordings, and immunofluorescence analysis.MethodsThe radial arm water maze and fear conditioning test were conducted to assess memory performance in PS19 mice with and without long-term LC stimulation. Hippocampal long-term potentiation (LTP) was recorded to evaluate the effect of long-term LC stimulation on synaptic plasticity. Immunofluorescence was employed to examine tau phosphorylation, neurodegeneration, and neuroinflammation.ResultsLong-term LC stimulation in PS19 mice exacerbated spatial memory deficits in the water maze, impaired contextual fear memory, reduced hippocampal LTP, and increased asparagine endopeptidase (AEP) expression, tau hyperphosphorylation, and neuroinflammation.ConclusionsLong-term LC stimulation may exacerbate memory deficits in PS19 mice by impairing synaptic plasticity and increasing neural degeneration in the hippocampus. Increased AEP expression and tau hyperphosphorylation in the LC further suggest a possible association between LC overactivation and AEP-associated tau pathology.</p>","PeriodicalId":14929,"journal":{"name":"Journal of Alzheimer's Disease","volume":" ","pages":"234-249"},"PeriodicalIF":3.4,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148520609","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Relation of fluid neurodegeneration biomarkers with white matter integrity in Alzheimer's disease patients in Latin America.","authors":"Thamires N C Magalhães, Raphael F Casseb, Adriel S Moraes, Camila V L Teixeira, Ana M Carletti, Thiago J R De Rezende, Helena P G Joaquim, Leda L Talib, Orestes Forlenza, Fernando Cendes, Marcio L F Balthazar, Charlotte E Teunissen","doi":"10.1177/13872877261467065","DOIUrl":"10.1177/13872877261467065","url":null,"abstract":"<p><p>BackgroundAlzheimer's disease (AD) is increasingly prevalent in Latin America. Neurofilament light chain (NfL) and glial fibrillary acidic protein (GFAP) are promising biomarkers of neurodegeneration, but their relationship with white matter (WM) integrity remains unclear.ObjectiveTo investigate associations between fluid neurodegeneration biomarkers and WM microstructure in a Brazilian cohort of individuals across the AD continuum and cognitively healthy controls.MethodsNinety-one participants were included: 27 cognitively healthy controls (mean age = 68.3 ± 5.2 years) and 64 amyloid-positive individuals with mild cognitive impairment or AD dementia (mean age = 70.6 ± 6.9 years). AD participants were characterized by low cerebrospinal fluid (CSF) Aβ₄₂ concentrations (<540 pg/mL) and altered Aβ₄₂/p-Tau and Aβ₄₂/t-Tau ratios. Serum and CSF concentrations of NfL and GFAP were measured using single-molecule array technology and examined in relation to diffusion tensor imaging metrics, including fractional anisotropy, mean diffusivity, radial diffusivity, and axial diffusivity (AxD).ResultsWithin the clinical AD group, higher serum NfL levels were associated with lower AxD in the left cingulum tract (r = -0.372, p = 0.007). In cognitively healthy controls, serum NfL showed positive correlations with AxD and mean diffusivity in the right cingulum (r = 0.650, p = 0.001 and r = 0.607, p = 0.003, respectively). No significant associations were observed between serum or CSF GFAP concentrations and diffusion tensor imaging metrics.ConclusionsSerum NfL was associated with anatomically specific WM microstructural changes, with differing patterns across clinical groups.</p>","PeriodicalId":14929,"journal":{"name":"Journal of Alzheimer's Disease","volume":" ","pages":"158-168"},"PeriodicalIF":3.4,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13499915/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148562120","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}