Journal of Alzheimer's Disease最新文献

{"title":"Association between atherogenic index of plasma and dementia: A longitudinal observational study.","authors":"Jie Lin, Yan Li, Hao Li","doi":"10.1177/13872877251339841","DOIUrl":"https://doi.org/10.1177/13872877251339841","url":null,"abstract":"<p><p>BackgroundAtherogenic index of plasma (AIP) is a novel biomarker for status of lipid metabolism, but the association between AIP and dementia remains unclear.ObjectiveWe aimed to investigate the association between AIP and dementia among people with different glycemic status.MethodsFrom the China Health and Retirement Longitudinal Study, 5195 dementia-free adults aged ≥45 (mean age 62.15 ± 7.00 years; 2668 [51.36%] female) at baseline (2011-2012) were followed up until 2018 to detect incident dementia. Dementia was ascertained based on cognitive batteries and the Activity of Daily Living scale. AIP was calculated by the formula: log [triglyceride (mg/dL) / high-density lipoprotein cholesterol (mg/dL)] and tertiled as low, moderate, and high. Data were analyzed using logistic regression.ResultsDuring the follow-up, 716 (13.3%) participants developed dementia. In basic-adjusted model, higher AIP was dose-dependently associated with an increased risk of dementia (per 1-SD increment in AIP, odds ratio [OR]: 1.10, 95% confidence interval [CI]: 1.02, 1.20, p = 0.020), whereas the association was not significant in fully-adjusted model (OR: 1.07 [0.97, 1.18]; p = 0.158). Compared with low AIP group, the OR (95% CI) of dementia was 1.27 (1.01, 1.60) for high AIP. After stratification, the association between high AIP and dementia was significant among people with diabetes (OR: 1.97, 95% CI: 1.11, 3.49) and a significant multiplicative interaction between high AIP and glycemic status was found (p for interaction = 0.029).ConclusionsHigh AIP is associated with higher risk of dementia, particularly among people with diabetes. Our findings suggested that AIP could serve as an early indicator of dementia.</p>","PeriodicalId":14929,"journal":{"name":"Journal of Alzheimer's Disease","volume":" ","pages":"13872877251339841"},"PeriodicalIF":3.4,"publicationDate":"2025-05-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143967526","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":"A critical examination of the relationship between cardiovascular health, cognition, and dementia risk.","authors":"Joshua L Gills, Omonigho M Bubu","doi":"10.1177/13872877251337776","DOIUrl":"https://doi.org/10.1177/13872877251337776","url":null,"abstract":"<p><p>Poor cardiovascular health is strongly linked to increased risk of cognitive impairment and Alzheimer's disease and related dementias. This commentary discusses Yang and associates' work on the associations between cardiovascular health in middle age, as defined by Life Essential 8 scores, and later digital cognitive performance and incident Alzheimer's disease. We examine the strengths and weaknesses of their study within the broader research context. We emphasize the potential significance of sleep and stress the need for longitudinal studies incorporating robust neuropsychiatric methodologies, advanced neuroimaging techniques, and diverse participant samples to enhance the reliability and generalizability of results.</p>","PeriodicalId":14929,"journal":{"name":"Journal of Alzheimer's Disease","volume":" ","pages":"13872877251337776"},"PeriodicalIF":3.4,"publicationDate":"2025-05-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144007182","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":"Use of posterior probabilities from a long short-term memory network for characterizing dance behavior with multiple accelerometers.","authors":"Aston K McCullough","doi":"10.1177/13872877251336482","DOIUrl":"https://doi.org/10.1177/13872877251336482","url":null,"abstract":"<p><p>BackgroundDancing may be protective for cognitive health among adults with mild cognitive impairment, Alzheimer's disease or dementia; however, additional methods are needed to characterize motor behavior quality in studies of dance.ObjectiveTo determine how long each of a range of motor behaviors should be observed to optimize the reliability of \"dance-like state\" (DLS) scores-a novel metric for characterizing motor behavior quality in reference to free-form dancing using accelerometry.MethodsAdults (<i>n</i> = 41) wore five triaxial accelerometers (on both wrists, both ankles, and the waist) while engaged in sitting, standing, walking, and free-form dancing in a laboratory. Accelerometer data were used as predictors in a long short-term memory (LSTM) network, where the target was the binary coded observed behavior (dancing/not dancing) over time. LSTM accuracy was evaluated, and the Spearman-Brown (SB) Prophecy formula was used to determine the number of 1-min observational periods required to reach sufficient reliability (<i>r</i> ≥ 0.80) when using DLS scores.ResultsThe LSTM network trained with accelerometer data that were collected using all five devices showed very good to excellent classification accuracy (95% confidence interval: 89.1% to 94.0%) in the task of recognizing free-form dance behavior. SB results showed LSTM-generated posterior probabilities are reliable (<i>r</i> > 0.80) when averaged over ≥2 min periods. DLS scores were significantly correlated with age, prior dance training, height, body mass, music tempo and mode, gait speed, and energy expenditure.ConclusionsDLS scores can be used to characterize motor behavior quality. Additional research on motor behavior quality in relation to cognitive health is needed.</p>","PeriodicalId":14929,"journal":{"name":"Journal of Alzheimer's Disease","volume":" ","pages":"13872877251336482"},"PeriodicalIF":3.4,"publicationDate":"2025-05-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143991259","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 emerging role of the circadian rhythm in the blood-brain barrier dysfunction associated with cerebral small vessel disease.","authors":"Yorito Hattori","doi":"10.1177/13872877251337775","DOIUrl":"https://doi.org/10.1177/13872877251337775","url":null,"abstract":"<p><p>The relationship between circadian rhythm and cerebrovascular disease has recently emerged as a fascinating area of research. It has been found that the circadian rhythm could affect the development and exacerbation of cerebral small vessel disease (CSVD). Dysfunction of the blood-brain barrier (BBB) is one of the key players in the mechanisms of CSVD. This is thought to be regulated by circadian oscillations of clock genes, which control transporter function, regulating the permeability of the BBB endothelial cells, tight junction proteins, and pericytes. Understanding the interaction between circadian genes and BBB components may contribute to the development of promising treatments for CSVD.</p>","PeriodicalId":14929,"journal":{"name":"Journal of Alzheimer's Disease","volume":" ","pages":"13872877251337775"},"PeriodicalIF":3.4,"publicationDate":"2025-05-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144014328","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":"DNA methylation age acceleration is associated with incident cognitive impairment in the health and retirement study.","authors":"Freida Blostein, Kelly M Bakulski, Mingzhou Fu, Herong Wang, Matthew Zawistowski, Erin B Ware","doi":"10.1177/13872877251333707","DOIUrl":"https://doi.org/10.1177/13872877251333707","url":null,"abstract":"<p><p>BackgroundDNA methylation clocks have emerged as promising biomarkers for cognitive impairment and dementia. Longitudinal studies exploring the association between DNA methylation clocks and cognitive decline have been constrained by limited sample sizes and a lack of diversity.ObjectiveOur study aimed to investigate associations between DNA methylation clocks and incident cognitive impairment using a larger and US nationally-representative sample from the Health and Retirement Study.MethodsWe measured DNA methylation age acceleration in 2016 by regressing the DNA methylation clocks, including GrimAge, against chronological age. Cognitive change over time was determined by Langa-Weir cognition status from 2016 to 2018. Multivariable logistic regression evaluated the association between DNA methylation age acceleration and cognitive change, adjusting for cell-type proportions, demographic, and health factors. We also applied inverse probability weighting to address potential selection bias from varying loss-to-follow-up rates.ResultsThe analytic sample (N = 2713) was 54% female, 8.4% Black/African American, 86% White, 7.5% Hispanic, and 68 years old at baseline. During the two years of follow-up, 12% experienced cognitive change and had higher baseline GrimAge (mean = 1.2 years) acceleration compared to those maintaining normal cognition (mean = -0.8 years). A one-year increase in GrimAge acceleration was associated with 1.05 times higher adjusted and survey-weighted odds of cognitive change during follow-up (95% CI: 1.01-1.10). This association was consistent after accounting for loss-to-follow-up (OR = 1.07, 95% CI: 1.04-1.11).ConclusionsOur study offers insights into DNA methylation age acceleration associated with cognitive change over time, suggesting avenues for improved prevention, diagnosis, and treatment.</p>","PeriodicalId":14929,"journal":{"name":"Journal of Alzheimer's Disease","volume":" ","pages":"13872877251333707"},"PeriodicalIF":3.4,"publicationDate":"2025-05-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144017699","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":"Smoking alters effective connectivity of resting-state brain networks in mild cognitive impairment.","authors":"Tianyi Zhang, Xiao Luo, Qingze Zeng, Kaicheng Li, Yi Chen, Yan Sun, Lumin Leng, Guoping Peng, Minming Zhang, Zhirong Liu","doi":"10.1177/13872877251333152","DOIUrl":"https://doi.org/10.1177/13872877251333152","url":null,"abstract":"<p><p>BackgroundSmoking, a modifiable risk factor for Alzheimer's disease (AD), is associated with impaired functional connectivity in resting-state networks (RSNs). This study investigates how smoking affects brain effective connectivity (EC).ObjectiveInvestigate smoking-associated EC alterations.MethodsWe identified 129 cognitively unimpaired (CU: 85 non-smokers, 44 smokers) and 84 mild cognitive impairment (MCI: 55 non-smokers, 29 smokers) participants. Granger causality analysis was used to calculate the directed interactions of information flows based on the seed areas of the default mode network, executive control network, and salience network. Mixed-effect analyses were performed to explore the interactive effects of smoking × cognitive status. Linear mixed-effects models evaluated correlations between EC values and longitudinal cognitive decline.ResultsMixed-effect analyses revealed significant interactive EC differences among 4 groups: (1) Smoking MCI individuals showed reduced EC from the left putamen to the frontoinsular cortex (FIC) compared to the smoking CU and non-smoking MCI group; (2) Non-smoking MCI subjects had lower EC from the dorsolateral prefrontal cortex (DLPFC) to the right inferior occipital gyrus (IOG) than non-smoking CU; (3) Smoking CU subjects exhibited increased EC from the DLPFC to the left middle cingulate cortex compared to the with the non-smoking CU and smoking MCI individuals. Additionally, EC_{Posterior cingulate cortex-to-IOG} and EC_{Putamen-to-FIC} significantly predicted MMSE and ADNI_EF scores over time, respectively.ConclusionsSmoking distinctly impacts EC within RSNs and overall brain function in both MCI and CU individuals, potentially reducing functional compensation in MCI. These results support smoking cessation as part of AD management strategies.</p>","PeriodicalId":14929,"journal":{"name":"Journal of Alzheimer's Disease","volume":" ","pages":"13872877251333152"},"PeriodicalIF":3.4,"publicationDate":"2025-05-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144019042","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":"Chronic gingivitis increases the risk of early-onset Alzheimer's disease.","authors":"Dongcan Mo, Xiaoling Li, Jing He, Xiaozuo Lin, Pingkai Wang, Yinan Zeng, Xiaoju Wu, LiuYu Liu, Li Chi, Man Luo","doi":"10.1177/13872877251336259","DOIUrl":"https://doi.org/10.1177/13872877251336259","url":null,"abstract":"<p><p>BackgroundPeriodontal disease has two types of inflammatory states: gingivitis and periodontitis. While studies suggest a link between periodontal disease and Alzheimer's disease (AD), current evidence is insufficient to establish causality. This study employed Mendelian randomization (MR) and bioinformatics to investigate causal relationships between gingivitis, periodontitis, and AD types, while identifying diagnostic biomarkers through transcriptome-based bioinformatics approaches.ObjectiveThis study aims to explore the causal relationship between periodontal disease and AD using MR combined with bioinformatics analysis, investigate potential pathogenesis, and construct/validate diagnostic biomarkers.MethodsExposures and outcomes were selected from the Open whole-genome association study. Causal relationships were assessed using inverse variance-weighted (IVW), MR-Egger, and other supplementary methods. Transcriptome sequencing datasets were downloaded from Gene Expression Omnibus datasets. Key pathways and functions were identified through Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analysis. Protein-protein interaction and LASSO regression were used to construct and evaluate the diagnostic signature for early-onset AD (EOAD). Gene Set Enrichment Analysis was applied to analyze gene set enrichment between high and low-risk groups.ResultsIVW showed a positive correlation (OR = 1.161, 95% CI = 1.011-1.332, p = 0.035), and MR-Egger validated this result (OR = 1.296, 95% CI = 1.020-1.645, p = 0.049). These findings suggest that chronic gingivitis may increase EOAD risk. Reverse analysis results were negative. Immune activation, angiogenesis, and blood-brain barrier damage link the two diseases. The Inter-alpha-trypsin inhibitor heavy chain H5 (<i>ITIH5</i>) gene and <i>TGFB</i> pathway emerged in MR and bioinformatics analyses. A gene signature composed of <i>ITIH5</i>, <i>MFAP4</i>, and <i>PRELP</i> shows potential for diagnosing EOAD.ConclusionsChronic gingivitis may be associated with an increased risk of EOAD.</p>","PeriodicalId":14929,"journal":{"name":"Journal of Alzheimer's Disease","volume":" ","pages":"13872877251336259"},"PeriodicalIF":3.4,"publicationDate":"2025-05-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144010007","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":"Investigating the effects of 40 Hz sound stimulation on Alzheimer's disease pathways: Modulation of amyloid-β42 secretion, tau phosphorylation, phagocytosis, and autophagy.","authors":"Yuan-Han Yang, Hsi-Wen Chang, Ching-Fang Chien, Tzyh-Chyuan Hour","doi":"10.1177/13872877251339774","DOIUrl":"https://doi.org/10.1177/13872877251339774","url":null,"abstract":"<p><p>BackgroundAlzheimer's disease (AD) is the main cause of dementia in an aging society. Previous studies have demonstrated that non-invasive light flicker and sound with gamma frequency oscillations can modulate AD-related pathology in AD mice, potentially improving patient outcomes. However, the molecular mechanism by which sound with gamma frequency oscillations inhibits the expression of amyloid-β_1-42 (Aβ₄₂) and the phosphorylation of tau, and modulating cell autophagy in nerve cells are still unclear.ObjectiveThis study aimed to explore the molecular effects of 40 Hz sound stimulation on AD-related pathways in a cellular model.MethodsWe designed a 40 Hz stimulating sound (H⁺ multi-frequency audio) for this study, and cells were exposed to H⁺ multi-frequency audio. The concentration of Aβ₄₂ was quantified by enzyme-linked immunosorbent assay. Protein levels were examined by western blotting. Phagocytosis was examined by confocal microscopy and phagocytic analysis.ResultsFirst, we found that exposure to the 40 Hz stimulating sound inhibited the secretion of Aβ₄₂ by activating the AβPP/ADAM10 pathway and suppressing the AβPP/BACE1 pathway. Second, 40 Hz stimulating sound inhibited tau phosphorylation at Thr181 through the inactivation of the Akt/mTOR pathway. Third, 40 Hz stimulating sound enhanced the phagocytosis and autophagy of Aβ₄₂ through the AMPK/ULK/LC3B pathway in cells.ConclusionsOur study showed that 40 Hz stimulating sound is involved in the inhibition of Aβ₄₂ secretion, p-Tau protein expression, and the promotion of phagocytosis and Aβ₄₂ autophagy in cells. We suggest that 40 Hz stimulating sound could be a potential intervention to attenuate AD progression in the future.</p>","PeriodicalId":14929,"journal":{"name":"Journal of Alzheimer's Disease","volume":" ","pages":"13872877251339774"},"PeriodicalIF":3.4,"publicationDate":"2025-05-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143966724","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":"Loss of WDR23 slows the rate of age-related cognitive decline with elevated amyloid burden.","authors":"Jiahui Liu, Chatrawee Duangjan, Nguyen M Phan, Sean P Curran","doi":"10.1177/13872877251339776","DOIUrl":"https://doi.org/10.1177/13872877251339776","url":null,"abstract":"<p><p>BackgroundWDR23 is a regulator of cellular proteostasis and oxidative stress response processes that are critically involved in the pathogenesis of Alzheimer's disease (AD). Dysregulation of these pathways can contribute to amyloid-β (Aβ) and tau pathologies, ultimately leading to cognitive impairment.ObjectiveWe explored the effects of <i>Wdr23</i> knockout on key AD-related pathologies, including transcriptomic changes, Aβ and tau pathology, and cognitive function in the 3xTg-AD mouse model of early onset familial AD.MethodsTranscriptomic analysis of hippocampal tissue was performed to identify <i>Wdr23</i>-dependent gene expression changes across age groups. Aβ and tau pathology was assessed via immunohistochemistry. Behavioral assays were conducted to determine cognitive function and locomotor activity.ResultsTranscriptomic data revealed an age-dependent effect of <i>Wdr23</i> knockout on gene expression, with enrichment of pathways related to cognition and synaptic plasticity, especially middle-age and aged mice. Interestingly, while <i>Wdr23</i> knockout exacerbated amyloid plaque accumulation in older mice, it did not impact tau pathology. Behaviorally, <i>Wdr23</i> knockout mice exhibited improved cognitive function and enhanced activity levels compared to wild-type counterparts, suggesting a dissociation between Aβ pathology and cognitive performance. Additionally, we observed age-related changes in NRF2 target gene activation but declined in <i>Wdr23</i> knockout mice over time.ConclusionsOur findings highlight a complex relationship between proteostasis, amyloid pathology, and cognitive outcomes in AD, warranting further investigation into the specific mechanisms by which <i>Wdr23</i> modulates these processes. This study suggests that targeting proteostasis pathways could offer potential therapeutic benefits, particularly in preserving cognitive function, even in the presence of amyloid pathology.</p>","PeriodicalId":14929,"journal":{"name":"Journal of Alzheimer's Disease","volume":" ","pages":"13872877251339776"},"PeriodicalIF":3.4,"publicationDate":"2025-05-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144005720","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":"Presence of chronic morbidities alters skeletal muscle health and amino acid kinetics in mild cognitive impairment.","authors":"Sofie M De Wandel, Nicolaas Ep Deutz, Sarah K Kirschner, Elise En Deutz, Laura E Ruebush, Mariëlle Pkj Engelen","doi":"10.1177/13872877251336618","DOIUrl":"https://doi.org/10.1177/13872877251336618","url":null,"abstract":"<p><p>BackgroundSkeletal muscle weakness and mild cognitive impairment (MCI) commonly occur with aging.ObjectiveWe examined whether presence of chronic morbidities in MCI is associated with specific alterations in muscle health, functional capacity, and whole body amino acid kinetics.MethodsA group of 247 older adults were stratified into MCI/non-MCI (Montreal Cognitive Assessment) and presence/absence of chronic diseases. We measured lean mass by dual-energy x-ray absorptiometry, strength by dynamometry, and functional capacity by 6-min walk test. Postabsorptive whole body production (WBP) of amino acids were assessed by pulse administration of a mixture of 18 amino acid stable isotopes.ResultsMCI was associated with lower lean mass, functional capacity (p < 0.003), and WBP of arginine, glycine, leucine, and phenylalanine to tyrosine conversion (reflecting net protein breakdown (net PB)) but higher WBP of taurine (all p < 0.05). Presence of chronic morbidities was associated with lower muscle strength, WBP of glycine, and net PB (p < 0.0001), but higher WBP of phenylalanine, glutamate, taurine, tryptophan, and leucine (all p < 0.05). MCI*chronic morbidity interactions were found for muscle strength and net PB (p < 0.0001), with the lowest values in MCI with chronic morbidities.ConclusionsPresence of MCI and chronic morbidities in the older population affect different markers of muscle health and functional decline. Individuals with both MCI and chronic morbidities are at increased risk for severe muscle weakness likely related to a severe downregulation of glycine production and net protein breakdown. Therefore, it is important to consider the presence of chronic morbidities when investigating muscle health and functional capacity in MCI.</p>","PeriodicalId":14929,"journal":{"name":"Journal of Alzheimer's Disease","volume":" ","pages":"13872877251336618"},"PeriodicalIF":3.4,"publicationDate":"2025-05-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143990846","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}