Alzheimer's & Dementia最新文献

{"title":"Why diabetes matters in dementia studies: Failure to account for diabetes status masks regional mitochondrial DNA copy number changes in human hippocampus, amygdala, and cerebellum in Alzheimer's disease","authors":"Aakruti Kaikini, Anqi Shi, Paul Francis, Russell Swerdlow, Claire Troakes, Jaimee Kennedy, Alan Hodgkinson, Afshan N. Malik","doi":"10.1002/alz.71870","DOIUrl":"https://doi.org/10.1002/alz.71870","url":null,"abstract":"INTRODUCTION Diabetes is a major risk factor for Alzheimer's disease (AD), and both diseases involve mitochondrial dysfunction. Changes in mitochondrial DNA (mtDNA) can influence energy metabolism, cellular signaling, and epigenetic programming, thereby affecting cellular health. We hypothesized that AD is associated with reduced mtDNA copy number (mtDNA‐CN) in vulnerable brain regions, and that diabetes modifies these changes. METHODS MtDNA‐CN was quantified by absolute quantitative polymerase chain reaction (qPCR) in post‐mortem hippocampus, amygdala, and cerebellum from cognitive controls (CCs), AD, and diabetes groups (CC+D, AD+D; <jats:italic>N</jats:italic> = 66–77). RESULTS MtDNA‐CN differed by region, being highest in amygdala, intermediate in hippocampus, and lowest in cerebellum (503, 421, and 160 copies/cell; <jats:italic>p</jats:italic> &lt; 0.0001). Pooled analyses showed modestly lower mtDNA‐CN in AD. However, inclusion of diabetes appeared to mask differences. Donors with diabetes (CC+D and AD+D combined) had higher mtDNA‐CN than non‐diabetic (CC and AD combined) in hippocampus (+37.5%; <jats:italic>p</jats:italic> = 0.0012), amygdala (+30.6%; <jats:italic>p</jats:italic> = 0.0057), and cerebellum (+48.5%; <jats:italic>p</jats:italic> = 0.0002). This diabetes‐associated increase was also present within AD, where AD+D had higher mtDNA‐CN than AD in all regions. Removal of diabetic donors showed that AD was associated with a 19%–30% lower mtDNA‐CN, reaching significance in the amygdala and cerebellum after correction for multiple testing. DISCUSSION We show that AD is associated with multiregional mtDNA‐CN loss most clearly in donors without diabetes, whereas diabetes is associated with higher mtDNA‐CN and can mask AD‐related mitochondrial changes. The functional significance of higher mtDNA‐CN in the diabetic brain remains unclear, but evidence that diabetes acts as an effect modifier has important implications for dementia studies.","PeriodicalId":7471,"journal":{"name":"Alzheimer's & Dementia","volume":"26 1","pages":""},"PeriodicalIF":14.0,"publicationDate":"2026-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149221387","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":"Analysis of dementia strategic plans in US states","authors":"Matthew Nesvet, Shannon Effler, Natalie Sutton, Zachary Hass, Elizabeth Baker, Kathleen T. Unroe","doi":"10.1002/alz.71814","DOIUrl":"https://doi.org/10.1002/alz.71814","url":null,"abstract":"State dementia strategic plans provide policy and practice recommendations to reduce the risk, progression, and impact of dementia. Yet there is little systematic understanding of the contents of state plans nor how they aim to influence dementia strategy. This article analyzes state dementia plans, identifying five underspecified dementia policy areas in recent state plans and inconsistency in how states monitor the implementation of plans for effectiveness.","PeriodicalId":7471,"journal":{"name":"Alzheimer's & Dementia","volume":"12 1","pages":""},"PeriodicalIF":14.0,"publicationDate":"2026-10-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149218581","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":"Attention-deficit/hyperactivity disorder polygenic risk score and incidence of cognitive impairment in older adults: A prospective multicohort study","authors":"Douglas Teixeira Leffa,&nbsp;Guilherme Bauer-Negrini,&nbsp;Livia Amaral,&nbsp;Bruna Bellaver,&nbsp;Pamela C. L. Ferreira,&nbsp;Guilherme Povala,&nbsp;Firoza Z. Lussier,&nbsp;João Pedro Ferrari-Souza,&nbsp;Ann D. Cohen,&nbsp;Dana L. Tudorascu,&nbsp;Samuele Cortese,&nbsp;Luis Augusto Rohde,&nbsp;Brooke S. G. Molina,&nbsp;Derek Archer,&nbsp;Tharick A. Pascoal","doi":"10.1002/alz.71770","DOIUrl":"10.1002/alz.71770","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> INTRODUCTION</h3>\u0000 \u0000 <p>Preliminary evidence suggests a link between attention-deficit/hyperactivity disorder (ADHD) and later-life cognitive impairment. Whether genetic risk for ADHD, estimated using an ADHD polygenic risk score (ADHD-PRS), is associated with incident cognitive impairment (mild cognitive impairment or Alzheimer's disease dementia) remains unknown.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> METHODS</h3>\u0000 \u0000 <p>We analyzed 7761 cognitively unimpaired (CU) older adults with whole-genome sequencing from eight cohorts participating in the Alzheimer's Disease Sequencing Project (ADSP).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> RESULTS</h3>\u0000 \u0000 <p>During follow-up, 1347 participants developed cognitive impairment. Ten-year cumulative incidence was 33.8% in the highest ADHD-PRS tertile versus 23.4% in the lowest. In Cox models, higher ADHD-PRS remained associated with greater risk of cognitive impairment after adjustment for education, apolipoprotein E (<i>APOE)</i> ε4 status, or vascular risk. PRSs for other major psychiatric disorders were not associated with cognitive impairment in the same analytic framework. In a subsample with biomarker data, the association was not modified by baseline amyloid-β status.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> DISCUSSION</h3>\u0000 \u0000 <p>These findings support ADHD-PRS as a novel correlate of cognitive impairment and vulnerability in aging.</p>\u0000 </section>\u0000 </div>","PeriodicalId":7471,"journal":{"name":"Alzheimer's & Dementia","volume":"22 10","pages":""},"PeriodicalIF":12.8,"publicationDate":"2026-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/alz.71770","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149172977","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":"Not all sitting is equal: Novel neuroimaging insights into mentally passive versus active sedentary behaviors","authors":"Mats Hallgren, André Werneck, Liye Zou, David W Dunstan, Neville Owen","doi":"10.1002/alz.71905","DOIUrl":"https://doi.org/10.1002/alz.71905","url":null,"abstract":"","PeriodicalId":7471,"journal":{"name":"Alzheimer's & Dementia","volume":"11 1","pages":""},"PeriodicalIF":14.0,"publicationDate":"2026-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149172975","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":"Air pollution is associated with sex-specific longitudinal changes in astrocytic and neuroinflammatory processes linked to cognitive decline in Alzheimer's disease at-risk individuals","authors":"Natalia Vilor-Tejedor,&nbsp;Blanca Rodríguez-Fernández,&nbsp;Patricia Genius,&nbsp;Alba Fernández-Bonet,&nbsp;Armand González-Escalante,&nbsp;Anna Brugulat-Serrat,&nbsp;Gonzalo Sanchez-Benavides,&nbsp;Irene Cumplido-Mayoral,&nbsp;Carolina Minguillón,&nbsp;Marta Cirach,&nbsp;Mark Nieuwenhuijsen,&nbsp;Gwendlyn Kollmorgen,&nbsp;Clara Quijano-Rubio,&nbsp;Henrik Zetterberg,&nbsp;Kaj Blennow,&nbsp;Arcadi Navarro,&nbsp;Marc Suárez-Calvet,&nbsp;Juan Domingo Gispert,&nbsp;for the ALFA study","doi":"10.1002/alz.71837","DOIUrl":"10.1002/alz.71837","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> INTRODUCTION</h3>\u0000 \u0000 <p>Air pollution is associated with dementia risk, but its role during preclinical Alzheimer's disease (AD) remains unclear.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> METHODS</h3>\u0000 \u0000 <p>We examined long-term residential exposure to traffic-related air pollution in 226 cognitively unimpaired middle-aged individuals at increased risk of AD from the ALzheimer's and FAmilies ALFA+ cohort (a nested longitudinal cohort within the ALzheimer's and Families parent cohort). Participants underwent baseline and 3-year follow-up cerebrospinal fluid (CSF) assessment of AD, neurodegeneration, astrocytic, microglial, and inflammatory biomarkers. Exposure to nitrogen dioxide (NO₂), particulate matter (PM)₁₀, PM_2.5, and PM_2.5 absorbance was estimated using land-use regression models. Sex-interaction and stratified analyses were performed. Mediation analyses evaluated cognitive and brain-age outcomes.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> RESULTS</h3>\u0000 \u0000 <p>Sex-dependent associations were observed between air pollution exposure and CSF inflammatory and astrocytic biomarkers. Higher exposure was associated with longitudinal increases in glial fibrillary acidic protein (GFAP) and interleukin (IL) -6, primarily in women. GFAP partially mediated associations between air pollution exposure and worsening executive and attentional performance.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> DISCUSSION</h3>\u0000 \u0000 <p>Findings support sex-specific astroglial and neuroinflammatory susceptibility to traffic-related air pollution in preclinical AD.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> TRIAL REGISTRATION</h3>\u0000 \u0000 <p>The ALFA+ study has been registered at ClinicalTrials.gov (10-06-2015, identifier: NCT02485730).</p>\u0000 </section>\u0000 </div>","PeriodicalId":7471,"journal":{"name":"Alzheimer's & Dementia","volume":"22 10","pages":""},"PeriodicalIF":12.8,"publicationDate":"2026-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13662957/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149178813","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":"Brain microstructure mediates the relationship between Alzheimer's proteinopathies and memory","authors":"Quentin Devignes, Patrick J. Pruitt, Kenneth Petscavage, Robert A. Koeppe, Roger L. Albin, Scott J. Peltier, Annalise Rahman‐Filipiak, Bruno Giordani, Alexandru D. Iordan, Benjamin M. Hampstead","doi":"10.1002/alz.71899","DOIUrl":"https://doi.org/10.1002/alz.71899","url":null,"abstract":"INTRODUCTION We examined how amyloid beta (Aβ) and tau accumulation affected gray matter (GM) microstructural integrity and how such alterations impacted memory. METHODS We tested voxel‐wise mediation models to examine the relationships between (1) positron emission tomography‐derived Aβ and tau accumulation and GM microstructural integrity assessed with neurite orientation dispersion and density imaging, (2) GM microstructural integrity and memory controlling for Aβ and tau, and (3) the indirect effect of Aβ and tau on memory through GM microstructural integrity in 194 participants with memory impairments. RESULTS Tau had a greater impact on GM microstructure than did Aβ. GM microstructural alterations in posterior cortical regions were associated with worse memory when controlling for Alzheimer's proteinopathies. GM microstructural alterations mediated the relationship between Alzheimer's proteinopathies and memory. DISCUSSION GM microstructural alterations have functional ramifications given their mediating effect on the relationship between Alzheimer's proteinopathies and memory and their association with worse memory beyond Alzheimer's proteinopathies.","PeriodicalId":7471,"journal":{"name":"Alzheimer's & Dementia","volume":"11 1","pages":""},"PeriodicalIF":14.0,"publicationDate":"2026-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149172998","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":"Structured exercise, cognitive–social engagement, and cognitive impairment-free life expectancy across four longitudinal aging cohorts","authors":"Xiangwei Li,&nbsp;Ying Liu,&nbsp;Junyu Sun,&nbsp;Hui Zhang,&nbsp;Yaqian Xu,&nbsp;Chongyu Ding,&nbsp;Yanting Zhang,&nbsp;Tianlang Tong,&nbsp;Zhaojun Wang,&nbsp;Wei Lyu,&nbsp;Xian Cui","doi":"10.1002/alz.71854","DOIUrl":"10.1002/alz.71854","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> INTRODUCTION</h3>\u0000 \u0000 <p>Whether cognitive–social engagement can compensate for insufficient structured exercise in cognitive aging remains unclear.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> METHODS</h3>\u0000 \u0000 <p>We harmonized repeated data from four aging cohorts across Asia, North America, and Europe. Structured exercise and cognitive–social engagement were cross-classified at each wave into low–low (LL), high exercise–low engagement (HL), low exercise–high engagement (LH), and high–high (HH). Cohort-specific Cox models and multistate life tables estimated incident cognitive impairment and cognitive impairment-free life expectancy.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> RESULTS</h3>\u0000 \u0000 <p>Cognitive impairment-free life expectancy from age 50 was 17.5, 23.2, 20.1, and 24.7 years for the low exercise + low cognitive-social engagement (LL), high exercise + low cognitive-social engagement (HL), low exercise + high cognitive-social engagement (LH), and high exercise + high cognitive-social engagement (HH) groups, respectively.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> DISCUSSION</h3>\u0000 \u0000 <p>Structured exercise and cognitive–social engagement showed combined, non-interchangeable benefits for cognitive aging. These findings support integrated lifestyle strategies for dementia prevention across diverse aging populations, health systems, and prevention settings worldwide.</p>\u0000 </section>\u0000 </div>","PeriodicalId":7471,"journal":{"name":"Alzheimer's & Dementia","volume":"22 10","pages":""},"PeriodicalIF":12.8,"publicationDate":"2026-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/alz.71854","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149172976","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":"Diffusion MRI reveals amyloid plaque–associated cellular signatures through spatial transcriptomic integration","authors":"Xinyue Han, Rui Hu, Xingjie Ping, Jie Chen, Juan Liu, Zhuoheng Liu, Xiaoming Jin, Xiang Gao, Mingquan Lin, Yi Zhao, Nian Wang","doi":"10.1002/alz.71908","DOIUrl":"https://doi.org/10.1002/alz.71908","url":null,"abstract":"INTRODUCTION Amyloid plaque deposition is a defining feature of Alzheimer's disease (AD), yet how plaque‐associated cellular alterations are reflected in noninvasive imaging remains unclear. METHODS We integrated high‐resolution diffusion magnetic resonance imaging (dMRI) with spatial transcriptomics (ST) in an AD mouse model. Spatial correlations were assessed across the whole brain and in disease–control and plaque–non‐plaque comparisons. Neural network models were trained to predict AD‐associated cell types from dMRI metrics. RESULTS dMRI metrics showed moderate spatial correlations ( <jats:italic>r</jats:italic> = −0.41 to 0.36) with oligodendrocyte‐ and neuron‐related gene expression. Disease–control comparisons revealed region‐specific MRI‐derived microstructural alterations aligned with transcriptional changes in microglia, astrocytes, oligodendrocytes, and neurons. Plaque‐rich regions exhibited distinct diffusion and susceptibility signatures associated with oligodendrocyte and microglial expression. Neural networks predicted spatial distributions of AD‐associated cell types with 80%–86% accuracy. DISCUSSION dMRI captures plaque‐associated cellular pathology and supports biologically informed interpretation of imaging contrasts in AD.","PeriodicalId":7471,"journal":{"name":"Alzheimer's & Dementia","volume":"21 1","pages":""},"PeriodicalIF":14.0,"publicationDate":"2026-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149130520","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":"Spatiotemporal heterogeneity and dynamic evolution of microglial glucose metabolic reprogramming in Alzheimer's disease","authors":"Yuan Chen, Fuyao Li, Junlei Zhang, Mingqing Wei, Jingnian Ni, Ting Li, Lulu Yao, Jinzhou Tian, Jing Shi","doi":"10.1002/alz.71909","DOIUrl":"https://doi.org/10.1002/alz.71909","url":null,"abstract":"Alzheimer's disease (AD) is accompanied by persistent disturbances in brain energy metabolism, and microglial glucose metabolic reprogramming constitutes an important link among pathological protein deposition, neuroinflammation, and impaired clearance. This review examines these metabolic changes across disease stages, brain regions, and plaque‐associated microenvironments and proposes a dynamic state‐composition model. In this model, microglia in different metabolic states coexist, and their relative proportions and spatial distribution change as AD progresses. In early disease or during active phagocytosis, some microglia show enhanced glycolytic and oxidative phosphorylation (OXPHOS) programs. Under persistent pathological stress, increased glucose uptake may not translate into effective energy production and can coexist with inflammation and impaired lipid metabolism. In late disease, microglia with reduced metabolic capacity and impaired phagocytosis become more prevalent. However, higher expression of OXPHOS‐related genes in some microglial states associated with tau pathology does not necessarily indicate improved mitochondrial respiration. These population‐level patterns do not imply that individual microglia follow a fixed sequence of metabolic changes. Longitudinal cell tracking and microglia‐specific metabolic flux measurements are needed to test this model and inform interventions tailored to disease stage and microglial state.","PeriodicalId":7471,"journal":{"name":"Alzheimer's & Dementia","volume":"3 1","pages":""},"PeriodicalIF":14.0,"publicationDate":"2026-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149130515","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":"Association between early‐life farming exposure and Alzheimer's disease neuropathological burden","authors":"W. Ryan Powell, Eleanna M. Melcher, Rachel C. Otte, Sarah Lim, Lauren Etter, Aly Pfaff, Amanda DeWitt, Adrienne R. S. Lee, Fred B. Ketchum, M. Shahriar Salamat, Christopher A. Bradfield, Stephen A. Goutman, Megan L. Zuelsdorff, Kelly M. Bakulski, Robert A. Rissman","doi":"10.1002/alz.71904","DOIUrl":"https://doi.org/10.1002/alz.71904","url":null,"abstract":"BACKGROUND Farming populations may face a disproportionate share of adverse exposures influencing Alzheimer's disease (AD), yet farming data are rarely connected to cohorts with characterized AD neuropathology. Whether early‐life exposure is related to AD neuropathology is limited. METHOD Brain donors from two Alzheimer's Disease Research Centers ( <jats:italic>N</jats:italic> = 1035; between 1986–2018) were included. US Census records were used to identify those with early‐life farming exposure (birth to 17 years old) and examined alongside AD neuropathology assessments. RESULT Early‐life farming exposure (≈ 17% of donors) was associated with 60% higher odds of AD neuropathological burden (odds ratio = 1.60, 95% confidence interval: 1.09–2.35) adjusting for age, sex, and year of death. CONCLUSION Findings suggest exposure to farming early in life is linked to increased levels of AD neuropathology. Deeper occupational and residential phenotyping is needed to identify the potential multiple, overlapping risk pathways, which may include cumulative and sensitive life stage exposure to chemical toxicants, hearing loss, and psychosocial hazards.","PeriodicalId":7471,"journal":{"name":"Alzheimer's & Dementia","volume":"467 1","pages":""},"PeriodicalIF":14.0,"publicationDate":"2026-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149130524","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}