Florian Lange, Diego L. Guarin, Esther Ademola, Dalia Mahdy, Gabriela Acevedo, Thorsten Odorfer, Joshua K. Wong, Jens Volkmann, Robert Peach, Martin Reich
{"title":"Computer vision uncovers three fundamental dimensions of levodopa-responsive motor improvement in Parkinson’s disease","authors":"Florian Lange, Diego L. Guarin, Esther Ademola, Dalia Mahdy, Gabriela Acevedo, Thorsten Odorfer, Joshua K. Wong, Jens Volkmann, Robert Peach, Martin Reich","doi":"10.1038/s41531-025-00999-w","DOIUrl":"https://doi.org/10.1038/s41531-025-00999-w","url":null,"abstract":"<p>We developed VisionMD, an AI computer vision platform, analyzing over 1200 clinical videos of Parkinson’s patients’ hand movements across 13 years. This large-scale, markerless analysis identified three kinematic domains (speed, consistency, timing/scale) reliably improved by levodopa. Our method offers objective, quantitative motor assessment, reducing subjectivity and enhancing reproducibility compared to traditional scales.</p><figure></figure>","PeriodicalId":19706,"journal":{"name":"NPJ Parkinson's Disease","volume":"16 1","pages":""},"PeriodicalIF":8.7,"publicationDate":"2025-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144164930","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":"Complement C4 exacerbates astrocyte-mediated neuroinflammation and promotes α-synuclein pathology in Parkinson’s disease","authors":"Wenkai Zou, Liang Kou, Yiming Wang, Zongjie Jin, Nian Xiong, Tao Wang, Yun Xia","doi":"10.1038/s41531-025-01005-z","DOIUrl":"https://doi.org/10.1038/s41531-025-01005-z","url":null,"abstract":"<p>Complement C4, implicated in neuroinflammation and synaptic dysfunction, plays a poorly defined role in Parkinson’s disease (PD). Here, we demonstrate elevated C4 levels in PD patient plasma and the substantia nigra of α-synuclein preformed fibril (α-syn PFF)-injected mice, correlating with disease severity. α-syn PFF treatment induces complement C4 expression, particularly in neurons, with astrocytes further enhancing this response. Complement C4 was found to amplify astrocytic inflammatory responses, leading to increased neuronal apoptosis and synaptic damage. Additionally, conditioned media from astrocytes treated with α-syn PFF and complement C4 accelerated α-syn aggregation and synaptic loss in cultured neurons. In vivo, complement C4 exacerbated motor dysfunction, dopaminergic neuronal loss, and α-syn pathology in α-syn PFF-injected mice. These findings reveal that complement C4 significantly contributes to the neuroinflammatory environment and α-syn pathology in PD, highlighting its potential as a therapeutic target for mitigating neurodegeneration in this disorder.</p>","PeriodicalId":19706,"journal":{"name":"NPJ Parkinson's Disease","volume":"1118 1","pages":""},"PeriodicalIF":8.7,"publicationDate":"2025-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144164929","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}
Xiaolu Li, Shuting Bu, Huize Pang, Hongmei Yu, Mengwan Zhao, Juzhou Wang, Yu Liu, Guoguang Fan
{"title":"Mapping striatal functional gradients and associated gene expression in Parkinson’s disease with continuous cognitive impairment","authors":"Xiaolu Li, Shuting Bu, Huize Pang, Hongmei Yu, Mengwan Zhao, Juzhou Wang, Yu Liu, Guoguang Fan","doi":"10.1038/s41531-025-01002-2","DOIUrl":"https://doi.org/10.1038/s41531-025-01002-2","url":null,"abstract":"<p>Cognitive impairment in Parkinson’s disease is closely tied to striatal dysfunction, yet the neurobiological interface between macroscale connectivity and molecular signatures remains unexplored. This study characterizes striatal gradient organization and its genetic underpinnings across PD cognitive trajectories. We analyzed functional connectivity gradients in 126 PD patients (spanning the cognitive spectrum from normal cognition to dementia) and 40 healthy controls, correlating spatial patterns with neurotransmitter architecture and transcriptomic profiles. Three distinct striatal gradients emerged: Gradient 1 remains stable throughout disease progression and partially aligns with canonical striatal subdivisions. Gradient 2 represents a spatial continuum closely linked to dopaminergic innervation and becomes most pronounced in the dementia stage. Gradient 3 corresponds to cortico-striatal connectivity patterns implicated in both early and advanced cognitive deficits. Spatial transcriptomic and neuroimaging correlation analyses identified significant associations between cortico-striatal gradient disruptions and specific gene expression patterns. These findings provide valuable insights into striatal macro- and microstructural changes in PD and their role in cognitive impairment.</p>","PeriodicalId":19706,"journal":{"name":"NPJ Parkinson's Disease","volume":"5 1","pages":""},"PeriodicalIF":8.7,"publicationDate":"2025-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144153484","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":"Chronic stress induces depression-like behaviors and Parkinsonism via upregulating α-synuclein","authors":"Danhao Xia, Min Xiong, Yingxu Yang, Xin Wang, Qiang Chen, Sheng Li, Lanxia Meng, Zhentao Zhang","doi":"10.1038/s41531-025-00998-x","DOIUrl":"https://doi.org/10.1038/s41531-025-00998-x","url":null,"abstract":"<p>Parkinson’s disease (PD) is a neurodegenerative disorder characterized by the aggregation of α-synuclein (α-syn) and the nigrostriatal dopaminergic neuronal degeneration. Depression is one of the most common non-motor symptoms of PD patients. However, the pathogenic connection between PD and depression is not well understood. Herein, we report that chronic stress upregulates the expression of α-syn in the mouse brain. Overexpression of α-syn in the hippocampus replicates depressive-like phenotypes, whereas the genetic deletion of α-syn enhances resistance to chronic stress. Furthermore, chronic stress in early life promoted the deposition of α-syn aggregates in a transgenic mouse model that overexpresses human A53T mutant α-syn (A53T mice). Chronic stress also exacerbated dopaminergic degeneration and motor impairments in A53T mice. Strikingly, α-syn inclusions were also observed in the brains of some aged non-transgenic mice subjected to chronic stress. Together, our findings suggest that chronic stress upregulates α-synuclein expression, resulting in depression-like behaviors and parkinsonism.</p>","PeriodicalId":19706,"journal":{"name":"NPJ Parkinson's Disease","volume":"58 1","pages":""},"PeriodicalIF":8.7,"publicationDate":"2025-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144153578","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}
Emil Johansson, Antoine Freuchet, Gregory P. Williams, Tanner Michealis, April Frazier, Irene Litvan, Jennifer G. Goldman, Roy N. Alcalay, David G. Standaert, Amy W. Amara, Natividad Stover, Edward A. Fon, Ronald B. Postuma, John Sidney, David Sulzer, Cecilia S. Lindestam Arlehamn, Alessandro Sette
{"title":"T cell responses towards PINK1 and α-synuclein are elevated in prodromal Parkinson’s disease","authors":"Emil Johansson, Antoine Freuchet, Gregory P. Williams, Tanner Michealis, April Frazier, Irene Litvan, Jennifer G. Goldman, Roy N. Alcalay, David G. Standaert, Amy W. Amara, Natividad Stover, Edward A. Fon, Ronald B. Postuma, John Sidney, David Sulzer, Cecilia S. Lindestam Arlehamn, Alessandro Sette","doi":"10.1038/s41531-025-01001-3","DOIUrl":"https://doi.org/10.1038/s41531-025-01001-3","url":null,"abstract":"<p>A role of the immune system in Parkinson’s disease (PD) progression has long been suspected due to the increased frequency of activated glial cells and infiltrating T cells in the substantia nigra. It was previously reported that PD donors have increased T cell responses towards PINK1 and α-synuclein (α-syn), two Lewy body-associated proteins. Further, T cell reactivity towards α-syn was highest closer to disease onset, highlighting that autoreactive T cells might play a role in PD pathogenesis. However, whether T cell autoreactivity is present during prodromal PD is unknown. Here, we investigated T cell responses towards PINK1 and α-syn in donors at high risk of developing PD (i.e. prodromal PD: genetic risk, hyposmia, and or REM sleep behavior disorder), in comparison to PD and healthy control donors. T cell reactivity to these two autoantigens was detected in prodromal PD at levels comparable to those detected in individuals with clinically diagnosed PD. Aligned with the increased incidence of PD in males, we found that males with PD, but not females, had elevated T cell reactivity compared to healthy controls. However, among prodromal PD donors, males and females had elevated T cell responses. These differing trends in reactivity highlights the need for further studies of the impact of biological sex on neuroinflammation and PD progression.</p>","PeriodicalId":19706,"journal":{"name":"NPJ Parkinson's Disease","volume":"4 1","pages":""},"PeriodicalIF":8.7,"publicationDate":"2025-05-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144145882","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}
Sen Zhang, Min Yan, Xing Jiang, Youhan Liu, Wen Ma, Ling Ding, Zhimin Lu, Ying Luo, Xuewen Tian, Qinglu Wang
{"title":"Oligodendrocyte-astrocyte crosstalk in Parkinson’s disease mediates neuronal ferroptosis via the FGF signaling pathway","authors":"Sen Zhang, Min Yan, Xing Jiang, Youhan Liu, Wen Ma, Ling Ding, Zhimin Lu, Ying Luo, Xuewen Tian, Qinglu Wang","doi":"10.1038/s41531-025-00995-0","DOIUrl":"https://doi.org/10.1038/s41531-025-00995-0","url":null,"abstract":"<p>Parkinson’s disease (PD), as a neurodegenerative disorder, is characterized primarily by damage to the central nervous system, accompanied by astrocyte dysfunction and the activation of ferroptosis. Recent studies have shown that oligodendrocytes also exhibit functional abnormalities in the brains of PD patients and are involved in the ferroptotic process. However, it remains unclear whether there is an interaction between oligodendrocytes and astrocytes and how they induce neuronal ferroptosis. Here, we employed single-nucleus sequencing and spatial transcriptomics to characterize the intercellular communication network between oligodendrocytes and astrocytes in the PD environment. Among these, astrocytes are the primary recipients of signals sent by oligodendrocytes in the FGF (Fibroblast growth factors) signaling pathway. In PD, the communication intensity is weakened, involving FGF1 and FGF9 and their receptors FGFR1, FGFR2, and FGFR3. Subsequently, we further validated the significant activation of mitochondrial oxidative phosphorylation processes within oligodendrocytes and astrocytes in PD mice, and that astrocytes might also involve the interaction of Mt1 and Ca<sup>2+</sup>. Additionally, we demonstrated a significant reduction in the number of DA neurons in the SN region and a notable activation of ferroptosis, alongside a significant decrease in the antioxidant pathway NRF2/SLC7A11/GPX4. In summary, our data elucidate that ferroptosis in the midbrain SN region preferentially occurs in astrocytes under the dysregulation of oligodendrocytes, leading to ferroptosis in DA neurons. Thus, our study highlights the crucial role of oligodendrocyte-astrocyte crosstalk in driving neuronal inactivation and inflammatory expansion in PD.</p>","PeriodicalId":19706,"journal":{"name":"NPJ Parkinson's Disease","volume":"14 1","pages":""},"PeriodicalIF":8.7,"publicationDate":"2025-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144123004","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}
Pekka Kallunki, Florence Sotty, Katarina Willén, Michal Lubas, Laurent David, Malene Ambjørn, Ann-Louise Bergström, Louise Buur, Ibrahim Malik, Steffen Nyegaard, Thomas Thiilmark Eriksen, Berit O. Krogh, Jeffrey B. Stavenhagen, Kathrine J. Andersen, Lars Ø. Pedersen, Ersoy Cholak, Edward N. van den Brink, Rik Rademaker, Tom Vink, David Satijn, Paul W.H.I. Parren, Søren Christensen, Line R. Olsen, Josefine N. Søderberg, Sandra Vergo, Allan Jensen, Jan Egebjerg, Pernille Gry Wulff-Larsen, Mikkel N. Harndahl, Dina S. M. Damlund, Kaare Bjerregaard-Andersen, Karina Fog
{"title":"Rational selection of the monoclonal α-synuclein antibody amlenetug (Lu AF82422) for the treatment of α-synucleinopathies","authors":"Pekka Kallunki, Florence Sotty, Katarina Willén, Michal Lubas, Laurent David, Malene Ambjørn, Ann-Louise Bergström, Louise Buur, Ibrahim Malik, Steffen Nyegaard, Thomas Thiilmark Eriksen, Berit O. Krogh, Jeffrey B. Stavenhagen, Kathrine J. Andersen, Lars Ø. Pedersen, Ersoy Cholak, Edward N. van den Brink, Rik Rademaker, Tom Vink, David Satijn, Paul W.H.I. Parren, Søren Christensen, Line R. Olsen, Josefine N. Søderberg, Sandra Vergo, Allan Jensen, Jan Egebjerg, Pernille Gry Wulff-Larsen, Mikkel N. Harndahl, Dina S. M. Damlund, Kaare Bjerregaard-Andersen, Karina Fog","doi":"10.1038/s41531-024-00849-1","DOIUrl":"https://doi.org/10.1038/s41531-024-00849-1","url":null,"abstract":"<p>Amlenetug (Lu AF82422) is a human monoclonal antibody targeting α-synuclein in clinical development for multiple system atrophy. We describe a series of studies that characterize its functional properties and supported its selection as a viable clinical candidate. Amlenetug inhibits seeding induced in mouse primary neurons by various α-synuclein fibrillar assemblies and by aggregates isolated from MSA brain homogenate. In vivo, both co-injection of amlenetug with α-synuclein assemblies in mouse brain and peripheral administration inhibit α-synuclein seeding. Amlenetug inhibits uptake of α-synuclein seeds as well as accumulation of C-terminal truncated α-synuclein seeds and demonstrates binding to monomeric, aggregated, and truncated forms of human α-synuclein. The epitope of amlenetug was mapped to amino acids 112-117 and further characterized by crystallographic structure analysis. Based on our data, we hypothesize that targeting α-synuclein will potentially slow further disease progression by inhibiting further pathology development but be without impact on established pathology and symptoms.</p>","PeriodicalId":19706,"journal":{"name":"NPJ Parkinson's Disease","volume":"45 1","pages":""},"PeriodicalIF":8.7,"publicationDate":"2025-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144113977","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":"Choroid plexus enlargement contributes to motor severity via regional glymphatic dysfunction in Parkinson’s disease","authors":"Linyu Liu, Qiang Weng, Qing Cai, Xintong Yu, Weibin Huang, Shaohua Xie, Yan Shi, Huiting Li, Yuxuan Zhang, Jianping Hu, Mengcheng Li, Guannan Chen, Ning Wang, Xiang Lin, Ying Fu, Yu Lin","doi":"10.1038/s41531-025-00971-8","DOIUrl":"https://doi.org/10.1038/s41531-025-00971-8","url":null,"abstract":"<p>Choroid plexus (CP) enlargement and glymphatic dysfunction have been implicated in neurodegeneration, but their roles in Parkinson’s disease (PD) remain unclear. This retrospective cross-sectional study examined associations among CP volume, perivascular spaces (PVS), and motor symptom severity in 123 PD patients stratified by disease stage. MRI quantified CP volume and PVS, including dilated PVS (dPVS), across brain regions. CP-dPVS correlations were stronger in early-stage PD. Region-specific analyses revealed CP volume was associated with PVS in the midbrain and basal ganglia. CP-dPVS correlations emerged in midbrain, basal ganglia, and centrum semiovale. Correlation matrix and mediation analyses together confirmed that only basal ganglia dPVS was both significantly correlated with motor symptoms and served as a mediator, accounting for 30.52% of the association between CP volume and motor severity. These findings suggest that CP enlargement contributes to motor severity in PD, in part through regional glymphatic dysfunction localized to the basal ganglia.</p>","PeriodicalId":19706,"journal":{"name":"NPJ Parkinson's Disease","volume":"40 1","pages":""},"PeriodicalIF":8.7,"publicationDate":"2025-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144113910","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}
Emma Packer,Héloïse Debelle,Harry G B Bailey,Rana Zia Ur Rehman,Alison J Yarnall,Lynn Rochester,Lisa Alcock,Silvia Del Din
{"title":"Systematic review of wearables assessing medication effect on motor function and symptoms in Parkinson's disease.","authors":"Emma Packer,Héloïse Debelle,Harry G B Bailey,Rana Zia Ur Rehman,Alison J Yarnall,Lynn Rochester,Lisa Alcock,Silvia Del Din","doi":"10.1038/s41531-025-00943-y","DOIUrl":"https://doi.org/10.1038/s41531-025-00943-y","url":null,"abstract":"To improve motor function and symptoms, people with Parkinson's (PwP) typically take dopaminergic medication. In PwP, wearable technology (WT) can provide objective insights into medication effect. This review aims to identify and explore literature which uses WT to quantify the effect of medication on motor function and symptoms in PwP (PROSPERO 2022 CRD42022310018). Nine databases were searched between January 2000-October 2024. Downs and Black quality appraisal assessed study quality. PRISMA guidelines were followed. Amongst the seventy-nine included studies, 50 different WTs were placed across 20 locations on the body, and medication effect was monitored on 13 different motor functions/symptoms. There was great heterogeneity amongst protocols, but many studies were performed in controlled environments, exploring short-term medication effects (ON vs OFF). Medication effect varied, improving certain variables, and having no effect on others. Future research should identify gold-standard protocols to explore medication effect in real-world settings, over prolonged periods.Registration and Protocol PROSPERO 2022 CRD42022310018.","PeriodicalId":19706,"journal":{"name":"NPJ Parkinson's Disease","volume":"46 1","pages":"135"},"PeriodicalIF":8.7,"publicationDate":"2025-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144122102","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}
Sherilyn Junelle Recinto, Alexandra Kazanova, Lin Liu, Brendan Cordeiro, Shobina Premachandran, Hicham Bessaiah, Alexis Allot, Elia Afanasiev, Sriparna Mukherjee, Jessica Pei, Adam MacDonald, Moein Yaqubi, Heidi M. McBride, Diana Matheoud, Louis-Eric Trudeau, Samantha Gruenheid, Jo Anne Stratton
{"title":"PINK1 deficiency rewires early immune responses in a mouse model of Parkinson’s disease triggered by intestinal infection","authors":"Sherilyn Junelle Recinto, Alexandra Kazanova, Lin Liu, Brendan Cordeiro, Shobina Premachandran, Hicham Bessaiah, Alexis Allot, Elia Afanasiev, Sriparna Mukherjee, Jessica Pei, Adam MacDonald, Moein Yaqubi, Heidi M. McBride, Diana Matheoud, Louis-Eric Trudeau, Samantha Gruenheid, Jo Anne Stratton","doi":"10.1038/s41531-025-00945-w","DOIUrl":"https://doi.org/10.1038/s41531-025-00945-w","url":null,"abstract":"<p>Parkinson’s disease is characterized by a period of non-motor symptoms, including gastrointestinal dysfunction, preceding motor deficits by several years to decades. This long prodrome is suggestive of peripheral immunity involvement in the initiation of disease. We previously developed a model system in PINK1 KO mice displaying PD-like motor symptoms at late stages following intestinal infections. Herein, we map the initiating immune events at the site of infection in this model. Using single-cell RNAseq, we demonstrate that peripheral myeloid cells are the earliest highly dysregulated immune cell type followed by an aberrant T cell response shortly after. We also demonstrate an increased propensity for antigen presentation and that activated myeloid cells acquire a proinflammatory profile capable of inducing cytotoxic T cell responses. Together, our study provides the first evidence that PINK1 is a key regulator of immune functions in the gut underlying early PD-related disease mechanisms.</p>","PeriodicalId":19706,"journal":{"name":"NPJ Parkinson's Disease","volume":"133 1","pages":""},"PeriodicalIF":8.7,"publicationDate":"2025-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144113909","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}
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