Miguel A. Labrador-Espinosa, Jesús Silva-Rodríguez, Pablo Mir, Michel J. Grothe
{"title":"Data-driven characterization of distinct cognitive subtypes in Parkinson’s disease dementia","authors":"Miguel A. Labrador-Espinosa, Jesús Silva-Rodríguez, Pablo Mir, Michel J. Grothe","doi":"10.1038/s41531-025-00970-9","DOIUrl":"https://doi.org/10.1038/s41531-025-00970-9","url":null,"abstract":"<p>Individual cognitive profiles of patients with Parkinson’s disease dementia (PDD) are highly heterogeneous, suggesting possible biological subtypes. We studied 75 PD patients who developed dementia in the course of the Parkinson’s Progression Markers Initiative study to investigate data-driven evidence for the existence of distinct cognitive subtypes of PDD. Using Ward’s hierarchical clustering on neuropsychological test data, we identified two distinct cognitive subtypes. Despite similar dementia severity (MoCA: 20.6 vs 20.0), cluster-A exhibited more pronounced memory deficits (<i>n</i> = 50), whereas cluster-B showed greater visuospatial impairments (<i>n</i> = 25). The subtypes did not differ in demographic, motor, or MRI-based neurodegeneration measures. However, the visuospatial-predominant cluster-B had a higher prevalence of GBA mutations (<i>p</i> = 0.003) and hallucinations (<i>p</i> = 0.009). No differences were found in APOE-ε4 prevalence or cerebrospinal fluid biomarkers of Alzheimer’s pathology. These findings reveal distinct memory-predominant and visuospatial-predominant PDD subtypes, which associate with different clinical and genetic features but are independent of comorbid Alzheimer’s pathology.</p>","PeriodicalId":19706,"journal":{"name":"NPJ Parkinson's Disease","volume":"50 1","pages":""},"PeriodicalIF":8.7,"publicationDate":"2025-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143930980","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}
Sinah Röttgen, Eva Schaeffer, Annette Rogge, Ramona Hartung, Konstantin Kufer, Gereon R. Fink, Daniela Berg, Anja Ophey, Michael Sommerauer
{"title":"The prodromal individuals’ perspective on active recruitment for early detection of α-synucleinopathies","authors":"Sinah Röttgen, Eva Schaeffer, Annette Rogge, Ramona Hartung, Konstantin Kufer, Gereon R. Fink, Daniela Berg, Anja Ophey, Michael Sommerauer","doi":"10.1038/s41531-025-00979-0","DOIUrl":"https://doi.org/10.1038/s41531-025-00979-0","url":null,"abstract":"<p>Only the timely detection of individuals with incipient α-synucleinopathies can pave the way for developing disease-modifying therapies. Our aim was to explore the views of individuals with isolated REM sleep behavior disorder (iRBD), actively recruited from the general population, on the ethical justifiability of active recruitment and their experiences with risk disclosure. This mixed-methods study surveyed individuals with iRBD, confirmed by video-polysomnography, utilizing an interdisciplinary-developed online questionnaire. Of 99 invited individuals, 75 (75.8%) answered the survey. While 55.6% experienced the information on the increased risk as burdensome, 63.9% supported risk disclosure if consent had been obtained beforehand. Almost all individuals (96.2%) regarded our active recruitment method as appropriate, and 86.7% indicated they would participate again. Open-text responses indicated that key motivations included access to information and care, and contributing to research progress. This well-received recruitment strategy could serve as a model for future screening initiatives in α-synucleinopathy research.</p>","PeriodicalId":19706,"journal":{"name":"NPJ Parkinson's Disease","volume":"1 1","pages":""},"PeriodicalIF":8.7,"publicationDate":"2025-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143930977","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}
Xiaoxi Jing, Zongzhi Liu, Wenwen Li, Kaiyan Ma, Jiaxiang Zhang, Zeqi Yan, Shuo Zhang, Jiecong Lin, Junpeng Zhao, Ken K. Ong, John R. B. Perry, Yajie Zhao
{"title":"Protein-truncating variants in UQCRC1 are associated with Parkinson’s disease: evidence from half-million people","authors":"Xiaoxi Jing, Zongzhi Liu, Wenwen Li, Kaiyan Ma, Jiaxiang Zhang, Zeqi Yan, Shuo Zhang, Jiecong Lin, Junpeng Zhao, Ken K. Ong, John R. B. Perry, Yajie Zhao","doi":"10.1038/s41531-025-00987-0","DOIUrl":"https://doi.org/10.1038/s41531-025-00987-0","url":null,"abstract":"<p>Recent studies have suggested a potential but inconsistent link between <i>UQCRC1</i> and Parkinson’s disease (PD). For the first time, we systematically investigated the association between non-synonymous variants in <i>UQCRC1</i> and PD risk using data from the UK Biobank with half-million participants, which provide evidence supporting the role of <i>UQCRC1</i> Protein-truncating variants (PTVs) in PD (<i>P</i> = 1.20 × 10<sup>−6</sup>, OR = 6.59) and highlight the importance of large-scale population studies in identifying rare genetic risk factors.</p>","PeriodicalId":19706,"journal":{"name":"NPJ Parkinson's Disease","volume":"56 1","pages":""},"PeriodicalIF":8.7,"publicationDate":"2025-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143930976","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}
Judie Tabbal, Aida Ebadi, Ahmad Mheich, Aya Kabbara, Bahar Güntekin, Görsev Yener, Veronique Paban, Ute Gschwandtner, Peter Fuhr, Marc Verin, Claudio Babiloni, Sahar Allouch, Mahmoud Hassan
{"title":"Characterizing the heterogeneity of neurodegenerative diseases through EEG normative modeling","authors":"Judie Tabbal, Aida Ebadi, Ahmad Mheich, Aya Kabbara, Bahar Güntekin, Görsev Yener, Veronique Paban, Ute Gschwandtner, Peter Fuhr, Marc Verin, Claudio Babiloni, Sahar Allouch, Mahmoud Hassan","doi":"10.1038/s41531-025-00957-6","DOIUrl":"https://doi.org/10.1038/s41531-025-00957-6","url":null,"abstract":"<p>Neurodegenerative diseases like Parkinson’s (PD) and Alzheimer’s (AD) exhibit considerable heterogeneity of functional brain features within patients, complicating diagnosis and treatment. Here, we use electroencephalography (EEG) and normative modeling to investigate neurophysiological mechanisms underpinning this heterogeneity. Resting-state EEG data from 14 clinical units included healthy adults (<i>n</i> = 499) and patients with PD (<i>n</i> = 237) and AD (<i>n</i> = 197), aged over 40. Spectral and source connectivity analyses provided features for normative modeling, revealing significant, frequency-dependent EEG deviations with high heterogeneity in PD and AD. Around 30% of patients exhibited spectral deviations, while ~80% showed functional source connectivity deviations. Notably, the spatial overlap of deviant features did not exceed 60% for spectral and 25% for connectivity analysis. Furthermore, patient-specific deviations correlated with clinical measures, with greater deviations linked to worse UPDRS for PD (<i>⍴</i> = 0.24, <i>p</i> = 0.025) and MMSE for AD (<i>⍴</i> = −0.26, <i>p</i> = 0.01). These results suggest that EEG deviations could enrich individualized clinical assessment in Precision Neurology.</p>","PeriodicalId":19706,"journal":{"name":"NPJ Parkinson's Disease","volume":"17 1","pages":""},"PeriodicalIF":8.7,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143920421","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}
Alessandro Gialluisi, Simona Costanzo, Maria Ilenia De Bartolo, Giovanni Veronesi, Matteo Renzi, Assuntina Cembalo, Alfonsina Tirozzi, Stefania Falciglia, Moreno Ricci, Americo Bonanni, Francesco Martone, Gaetano Zazzaro, Antonietta Pepe, Daniele Belvisi, Marco Mario Ferrario, Francesco Gianfagna, Chiara Cerletti, Maria Benedetta Donati, Stefania Massari, Alfredo Berardelli, Giovanni de Gaetano, Licia Iacoviello
{"title":"Prominent role of PM10 in the link between air pollution and incident Parkinson’s Disease","authors":"Alessandro Gialluisi, Simona Costanzo, Maria Ilenia De Bartolo, Giovanni Veronesi, Matteo Renzi, Assuntina Cembalo, Alfonsina Tirozzi, Stefania Falciglia, Moreno Ricci, Americo Bonanni, Francesco Martone, Gaetano Zazzaro, Antonietta Pepe, Daniele Belvisi, Marco Mario Ferrario, Francesco Gianfagna, Chiara Cerletti, Maria Benedetta Donati, Stefania Massari, Alfredo Berardelli, Giovanni de Gaetano, Licia Iacoviello","doi":"10.1038/s41531-025-00935-y","DOIUrl":"https://doi.org/10.1038/s41531-025-00935-y","url":null,"abstract":"<p>Air pollution has been associated with Parkinson’s Disease (PD) risk, although this relationship remains unclear. We estimated yearly levels of exposure to ten air pollutants (period 2006–2018) in an Italian population cohort, the Moli-sani study (<i>N</i> = 24,325; ≥35 years; 51.9% women), and derived three principal components, testing their associations with incident PD risk over 23,841 participants (213 cases, median(IQR) follow-up 11.2(2.0) years). This revealed a statistically significant association of PC1 (explaining 38.2% of common variance, tagging PM10 levels), independent on sociodemographic, professional and lifestyles covariates (Hazard Ratio [95%CI] = 1.04[1.02–1.07]). The association was confirmed testing average PM10 levels during follow-up (18[13–24]% increase of PD risk per 1 μg/m<sup>3</sup> increase of PM10). Among different circulating markers, lipoprotein a explained a significant proportion of this association (2.8[0.9; 8.4]%). These findings suggest PM10 as a target to lower PD risk at the population level and a potential implication of lipoprotein a in PD etiology.</p>","PeriodicalId":19706,"journal":{"name":"NPJ Parkinson's Disease","volume":"81 1","pages":""},"PeriodicalIF":8.7,"publicationDate":"2025-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143915320","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}
Christopher F. Madelung, Annemette Løkkegaard, Søren A. Fuglsang, Marta M. Marques, Vincent O. Boer, Kristoffer H. Madsen, Anne-Mette Hejl, David Meder, Hartwig R. Siebner
{"title":"High-resolution mapping of substantia nigra in Parkinson’s disease using 7 tesla magnetic resonance imaging","authors":"Christopher F. Madelung, Annemette Løkkegaard, Søren A. Fuglsang, Marta M. Marques, Vincent O. Boer, Kristoffer H. Madsen, Anne-Mette Hejl, David Meder, Hartwig R. Siebner","doi":"10.1038/s41531-025-00972-7","DOIUrl":"https://doi.org/10.1038/s41531-025-00972-7","url":null,"abstract":"<p>Parkinson’s disease causes a progressive loss of dopaminergic neurons and iron accumulation in the substantia nigra pars compacta. Using ultra-high field magnetic resonance imaging (MRI) at 7 tesla in 43 Parkinson’s patients and 24 healthy controls, we analyzed the voxel-wise pattern of structural disintegration of dopamine neurons with neuromelanin-sensitive MRI, along with assessing iron accumulation using R2* and quantitative susceptibility mapping (QSM). We also explored correlations between these measures and the severity of residual motor symptoms in the on-medication state and other clinical variables. Differences were most notable in the nigrosomes within the pars compacta, with patients showing reduced neuromelanin signals and increased QSM values. Severity and asymmetry of motor symptoms correlated with higher R2* and QSM values in nigrosome N1. Thus, ultra-high field MRI provides high-resolution maps of various aspects of the underlying neurodegenerative process which reflect individual motor impairment in Parkinson’s disease.</p>","PeriodicalId":19706,"journal":{"name":"NPJ Parkinson's Disease","volume":"98 1","pages":""},"PeriodicalIF":8.7,"publicationDate":"2025-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143909981","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}
Juyoung Jenna Yun, Subati Abulikemu, Kodchakorn Love Jangwanich, Yen F. Tai, Shlomi Haar
{"title":"Modulatory effect of levodopa on the basal ganglia-cerebellum connectivity in Parkinson’s disease","authors":"Juyoung Jenna Yun, Subati Abulikemu, Kodchakorn Love Jangwanich, Yen F. Tai, Shlomi Haar","doi":"10.1038/s41531-025-00954-9","DOIUrl":"https://doi.org/10.1038/s41531-025-00954-9","url":null,"abstract":"<p>Long-term levodopa use in Parkinson’s disease is associated with declining efficacy and motor complications. Understanding its effects on brain reorganisation is vital for optimizing therapy. Using data from Parkinson’s Progression Marker Initiative, we investigated levodopa’s impact on resting-state functional connectivity within the cortico-basal ganglia-cerebellum system in 29 patients, under drug-naïve and levodopa-medicated conditions. Univariate comparisons of inter-regional connectivity between conditions were conducted, and multivariate combinations of connections within and between networks were assessed. No significant effect of levodopa was found using the univariate seed-based approach. However, the network connectivity pattern between basal ganglia and cerebellum showed robust classification power. Eigenvector Centrality Mapping (ECM) further identified functional hubs, with cerebellar hubs being the only ones within the cortico-basal ganglia-cerebellum system affected by medication. Our study provides further insight into the importance of inter-network functional connectivity in Parkinson’s and the impact of levodopa medication, highlighting the often-overlooked role of the cerebellum.</p>","PeriodicalId":19706,"journal":{"name":"NPJ Parkinson's Disease","volume":"39 1","pages":""},"PeriodicalIF":8.7,"publicationDate":"2025-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143915321","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}
Leslie C Jellen,Martha L Escobar Galvis,Qiong Sha,Christine Isaguirre,Amy Johnson,Zach Madaj,Mechelle M Lewis,Ryan D Sheldon,Lan Kong,Xuemei Huang,Lena Brundin
{"title":"Sex differences in peripheral and central dysregulation of the kynurenine pathway in Parkinson's disease.","authors":"Leslie C Jellen,Martha L Escobar Galvis,Qiong Sha,Christine Isaguirre,Amy Johnson,Zach Madaj,Mechelle M Lewis,Ryan D Sheldon,Lan Kong,Xuemei Huang,Lena Brundin","doi":"10.1038/s41531-025-00949-6","DOIUrl":"https://doi.org/10.1038/s41531-025-00949-6","url":null,"abstract":"We previously demonstrated that kynurenine pathway (KP) dysregulation associates with Parkinson's disease (PD) and its symptoms. Here, we profiled 16 KP-related markers in a second, independent cohort; plasma: n = 202 (116 PD (\"OFF\"), 86 controls); CSF: n = 183 (108, 75). Consistent with previous findings, we detected significantly higher concentrations of neurotoxic 3-hydroxykynurenine in plasma and lower concentrations of neuroprotective kynurenic acid along with higher neurotoxic quinolinic acid/kynurenic acid ratios in CSF of PD patients. Additionally, 10 markers showed sex-based differences, with more pronounced dysregulation in females. These 10 markers loaded to a single principal component linked to higher UPDRS I and II scores. Together, this suggests a composite signature of KP dysregulation in PD that is associated with worse symptoms and more prevalent in women. This work shows that KP dysregulation in peripheral and central compartments is linked to symptom severity in PD and warrants further systematic studies unraveling sex-dependent metabolic differences.","PeriodicalId":19706,"journal":{"name":"NPJ Parkinson's Disease","volume":"16 1","pages":"116"},"PeriodicalIF":8.7,"publicationDate":"2025-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143914990","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}
Xiaoman Yang, Zhuoran Ma, Piaopiao Lian, Yi Wu, Ke Liu, Zhaoyuan Zhang, Zhicheng Tang, Yan Xu, Xuebing Cao
{"title":"Disruption of axonal transport in Parkinson’s disease: the role of pathological α-Syn and AMPK/p38 MAPK signaling","authors":"Xiaoman Yang, Zhuoran Ma, Piaopiao Lian, Yi Wu, Ke Liu, Zhaoyuan Zhang, Zhicheng Tang, Yan Xu, Xuebing Cao","doi":"10.1038/s41531-025-00926-z","DOIUrl":"https://doi.org/10.1038/s41531-025-00926-z","url":null,"abstract":"<p>The accumulation of α-synuclein within Lewy bodies is a critical factor in the pathogenesis of Parkinson’s disease, with potential implications for axonal transport deficits. Activated asparagine endopeptidase enzymatically cleaves α-synuclein and tau, resulting in the formation of α-SynN103 and tauN368, which are markedly elevated in the brains with Parkinson’s disease. In this study, rats received intrastriatal injections of 15 µg of preformed α-SynN103 and tauN368 fibrils, and their behaviors were evaluated after a 2-month period. Subsequent analyses investigated alterations in axonal transport and the underlying molecular mechanisms. Our findings indicated that preformed fibrils reduced kinesin levels and excessively activated the AMPK and p38 MAPK, thereby compromising the function of kinesin and dynein in axonal transport. Pharmacological inhibition of AMPK and p38 MAPK ameliorated these dysfunctions in rat models, which identified Compound C and SB203580 as potent inhibitors, offering evidence for early interventions of Parkinson’s disease.</p><figure><p>Mechanisms by which PFFs caused axonal transport defects of dopamine neurons in PD-like models. (A) Shows normal axonal transport. (B) Demonstrates how PFFs increase ?-Syn accumulation, reducing PIKE expression and triggering AMPK/p38 MAPK over-activation, which lowers kinesin levels and motor-cargo interaction. (C) AMPK activity inhibition with C.C significantly improves these deficits. (D) The p38 inhibitor enhances kinesin transport by preventing p38 MAPK over-activation, reducing its inhibition of kinesin-cargo binding.</p></figure>","PeriodicalId":19706,"journal":{"name":"NPJ Parkinson's Disease","volume":"15 1","pages":""},"PeriodicalIF":8.7,"publicationDate":"2025-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143909979","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}
Hong-Qi Yang, Ran Xin, Ning-Ning Che, Qiu-Huan Jiang, Shuai Chen, Si-Yuan Chen, Zhi-Kun Sun, Wei-Min Yang, Xue Li, Jian-Jun Ma, Jie-Wen Zhang, Rayaz A. Malik
{"title":"Corneal confocal microscopy differentiates patients with secondary parkinsonism from idiopathic Parkinson’s disease","authors":"Hong-Qi Yang, Ran Xin, Ning-Ning Che, Qiu-Huan Jiang, Shuai Chen, Si-Yuan Chen, Zhi-Kun Sun, Wei-Min Yang, Xue Li, Jian-Jun Ma, Jie-Wen Zhang, Rayaz A. Malik","doi":"10.1038/s41531-025-00969-2","DOIUrl":"https://doi.org/10.1038/s41531-025-00969-2","url":null,"abstract":"<p>Parkinson’s disease (PD) is characterized by progressive degeneration of dopaminergic neurons in the substantia nigra, while secondary parkinsonism (SP) may be due to drugs, vascular, infectious, inflammatory, or even paraneoplastic etiologies. There is currently no biomarker that accurately distinguishes SP from PD. Corneal confocal microscopy (CCM) identifies corneal nerve loss which is associated with motor, cognitive and autonomic dysfunction in PD patients. This study enrolled participants with PD (<i>n</i> = 45) and SP (<i>n</i> = 25). A subset of patients underwent L-6-<sup>18</sup>F-fluoro-3,4-dihydroxyphenylalanine (<sup>18</sup>F-DOPA) positron emission tomography (PET) scan which showed bilateral decreased dopamine uptake in the putamen and caudate of patients with PD, but not in those with SP. Corneal nerve fiber density (CNFD) (<i>P</i> < 0.001) was lower and corneal nerve branch density (CNBD) (<i>P</i> = 0.007) was higher in the PD group compared to the SP group. The receiver operating characteristic (ROC) analysis revealed that combined CNFD and CNBD showed excellent discrimination between SP and PD, with an area under the curve (AUC) of 0.924. CCM may have clinical utility in differentiating patients with SP from PD.</p>","PeriodicalId":19706,"journal":{"name":"NPJ Parkinson's Disease","volume":"281 1","pages":""},"PeriodicalIF":8.7,"publicationDate":"2025-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143909978","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}