Ageing Research Reviews最新文献

{"title":"The rise and deceleration of neuronal excitability in aging and Alzheimer’s disease: Mechanisms, implications, and therapeutic targets","authors":"Osvaldo Delbono , Zhong-Min Wang, María Laura Messi","doi":"10.1016/j.arr.2025.102999","DOIUrl":"10.1016/j.arr.2025.102999","url":null,"abstract":"<div><div>Neuronal hyperexcitability—defined as increased likelihood of action potential firing in response to stimuli—has emerged as a key pathophysiological feature in both normal aging and Alzheimer’s disease (AD). This review synthesizes current evidence across species and models, evaluating the prevalence, mechanisms, and consequences of heightened excitability at the cellular and network levels. We examine electrophysiological and imaging-based indicators of hyperexcitability, including enhanced spontaneous firing, increased calcium transients, and subclinical epileptiform activity. Data from rodent models and human studies reveal that hyperexcitability arises early in aging and AD, affecting key regions such as the hippocampus, prefrontal cortex, locus coeruleus, and spinal motor circuits. Importantly, this phenomenon is not uniformly pathological: some aged individuals, including so-called “super-agers,” retain stable excitability profiles, suggesting the existence of protective mechanisms. We further explore the functional impact of hyperexcitability, including impaired cognitive encoding, gait disturbances, muscle fatigue, and neuromuscular junction degradation. In the later stages of the disease, neuronal activity tends to shift toward hypoexcitability or shows a deceleration of prior hyperexcitability, primarily driven by progressive synaptic loss, accumulation of tau pathology, and metabolic failure. Current gaps in knowledge include the lack of longitudinal data, limited translation from animal models, and insufficient understanding of compensatory vs. detrimental excitability shifts. Emerging strategies—ranging from pharmacological modulation to neuromodulation and metabolic interventions—offer potential therapeutic avenues. We propose future directions including computational modeling, humanized chimeric models, and excitability biomarkers to guide intervention. Overall, neuronal hyperexcitability represents both a biomarker and modifiable contributor to aging- and AD-related decline. Its study offers a window into early-stage dysfunction and a target for disease-modifying interventions. This review critically examines the emerging evidence for neuronal hyperexcitability as a defining feature of brain aging and AD. We begin by clarifying the concept of hyperexcitability and outlining key cellular and network-level indicators used to detect it. We then synthesize findings on hyperexcitability in aging individuals, both human and animal, and extend this analysis to AD, highlighting overlapping and divergent mechanisms. A focused section explores how motor neuron hyperexcitability contributes to functional decline, followed by a discussion of the transition from early hyperexcitability to late deceleration of neuronal excitability across disease progression. Comparative insights across species and models are provided to underscore translational relevance. We also address current limitations and propose novel investigative directions,","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"114 ","pages":"Article 102999"},"PeriodicalIF":12.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145812320","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":"From genes to lifestyle: A multi-dimensional framework for Alzheimer’s disease prevention and therapy","authors":"Lining Su ,&nbsp;Yanbing Wang","doi":"10.1016/j.arr.2025.102947","DOIUrl":"10.1016/j.arr.2025.102947","url":null,"abstract":"<div><div>Alzheimer’s disease (AD) is a complex neurodegenerative disorder driven by multilayered molecular and cellular mechanisms that cannot be fully elucidated through single-omics approaches. Consequently, large-scale multi-omics integration-encompassing transcriptomics, epigenomics (e.g., methylation), and genetic association studies (GWAS/eQTL/mQTL)-has uncovered critical genetic and epigenetic networks underlying disease risk and progression.Based on these integrative insights, this review emphasized several genes-including KLHL21, SCN2B, ZNF415, and PITRM1-as potential contributors to AD pathogenesis. Notably, single-cell and spatial transcriptomics analyses revealed specific enrichment of these genes in astrocytes, underscoring the pivotal role of this cell type in Aβ clearance, tau propagation, and neuroinflammation. Exercise interventions were shown to selectively modulate the expression of these genes, providing molecular support for the preventive and therapeutic potential of non-pharmacological lifestyle strategies. Drug repurposing analyses using DrugBank have identified promising therapeutic candidates, including FDA-approved agents (e.g., valproic acid, raloxifene, and clomipramine) and naturally derived compounds (e.g., quercetin and fisetin), which may modulate key AD-related pathways. Furthermore, emerging evidence of miRNA-gene regulatory networks suggested an additional layer of post-transcriptional control that may regulate responses to pathological stimuli. Collectively, these integrative insights advocated for a multidimensional precision medicine framework that spans genetic, cellular,network, and lifestyle levels of regulation. This shift from single-target therapeutics to an integrated “gene-cell-network-lifestyle” paradigm open new theoretical and translational avenues for delaying or mitigating AD progression.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"113 ","pages":"Article 102947"},"PeriodicalIF":12.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145575072","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":"The role of DEAD-box helicases in cardiovascular diseases","authors":"Haiyang Ni ,&nbsp;Mingyu Wang ,&nbsp;QiZhu Tang","doi":"10.1016/j.arr.2025.103004","DOIUrl":"10.1016/j.arr.2025.103004","url":null,"abstract":"<div><div>Cardiovascular diseases (CVDs) remain the leading cause of global morbidity and mortality, characterized by complex pathological mechanisms involving myocardial metabolic disorders, vascular dysfunction, and uncontrolled inflammation. DEAD-box (DDX) helicases, a large family of RNA helicases within Superfamily 2 (SF2), are increasingly recognized as pivotal regulators of RNA metabolism, including transcription, splicing, translation, and degradation, via their conserved helicase core and variable terminal domains. Beyond maintaining RNA homeostasis, DDX helicases participate in diverse cellular processes such as cell proliferation, immunity, and stress responses, with emerging roles in CVD pathogenesis.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"114 ","pages":"Article 103004"},"PeriodicalIF":12.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145844543","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":"The role of in silico and in vitro models in Parkinson’s disease: Drug discovery and therapy applications","authors":"Munabize Himwaba ,&nbsp;Kermue Vasco Jarnda ,&nbsp;Maxwell Tarwin Dweh ,&nbsp;Xuan Liu ,&nbsp;Yuyue Xiang ,&nbsp;Xiyan Zou ,&nbsp;Hanxiao Lv ,&nbsp;Tianjiao Li ,&nbsp;Xinya Tu ,&nbsp;Jianwu Wang","doi":"10.1016/j.arr.2025.102953","DOIUrl":"10.1016/j.arr.2025.102953","url":null,"abstract":"<div><div>Parkinson's disease is a neurodegenerative condition, marked by a progressive deterioration in both motor and non-motor abilities, which can severely affect the quality of life of the elderly population. With no cure available, innovative tools in treatment development and drug discovery are necessary. For several years, traditional models have been essential; however, they face limitations in replicating the complex setting of Parkinson's disease. In this regard, in silico and in vitro models have become essential tools in advancing Parkinson's disease drug discovery because of the potential they exhibit over traditional models. Here, we comprehensively review the latest innovations in both models and discuss their role in discovering therapeutic targets, optimizing drug candidates, promoting personalized medicine, and identifying biomarkers. While in vitro models better simulate the complicated cell interactions and increase the predictability of therapeutic effects, silico models shine in cost-effectiveness and high-throughput drug screening. Additionally, we discuss how combining advanced technologies with both models can help to overcome current constraints and problems in Parkinson's disease drug discovery, therefore facilitating the development of effective and targeted therapies in a shorter timeframe.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"113 ","pages":"Article 102953"},"PeriodicalIF":12.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145598263","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":"Prevalence of frailty in cardiac transthyretin amyloidosis: A systematic review and meta-analysis","authors":"Alberto Finazzi ,&nbsp;Emma Esposito ,&nbsp;Chiara Riva ,&nbsp;Elisabetta Mangili ,&nbsp;Lorenzo Lodovici ,&nbsp;Adriana Antonella Bruni ,&nbsp;Elena Pinardi ,&nbsp;Maria Cristina Ferrara ,&nbsp;Daniela Pini ,&nbsp;Antonella Zambon ,&nbsp;Francesco Musca ,&nbsp;Stefano Perlini ,&nbsp;Chukwuma Okoye ,&nbsp;Giuseppe Bellelli","doi":"10.1016/j.arr.2025.102903","DOIUrl":"10.1016/j.arr.2025.102903","url":null,"abstract":"<div><h3>Background</h3><div>Cardiac amyloidosis (CA) is an increasingly recognized cause of heart failure. Frailty is common among older adults and strongly associated with adverse outcomes. However, its prevalence and clinical relevance in the context of CA have not been systematically examined. This review aimed to assess the prevalence of frailty in CA and qualitatively synthesize the evidence on its association with clinical outcomes.</div></div><div><h3>Methods</h3><div>A systematic review and meta-analysis of observational studies was conducted to assess frailty prevalence in CA. Databases searched included Embase, PubMed, CINAHL, Cochrane Library, and Google Scholar up to April 15, 2025. Studies reporting frailty prevalence in CA patients were included. Six assessors independently screened the articles, extracted data, and resolved conflicts by consensus. The methodological quality of the included studies was assessed using the Newcastle-Ottawa Scale.</div></div><div><h3>Results</h3><div>Out of 565 articles identified, six studies met inclusion criteria, including a total of 1422 participants with cardiac transthyretin amyloidosis (ATTR-CA). Reported frailty prevalence ranged from 14.5 % to 75 %, depending on the assessment method. A meta-analysis restricted to studies using the Clinical Frailty Scale (N = 1164) yielded a pooled frailty prevalence of 66 % (95 % CI, 57–74 %), with substantial heterogeneity (I² = 89.1 %). Frailty was consistently associated with higher mortality and poorer quality of life.</div></div><div><h3>Conclusions</h3><div>Frailty is highly prevalent in individuals with ATTR-CA and is independently associated with adverse clinical outcomes. These findings support the routine evaluation of frailty in the management of individuals with CA. PROSPERO registration (CRD42024607807).</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"113 ","pages":"Article 102903"},"PeriodicalIF":12.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145236092","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":"Glymphatic dysfunction in Parkinson's disease: Aging-associated impairments, imaging biomarkers, and therapeutic strategies","authors":"Yan Lv ,&nbsp;Xv-Shen Ding ,&nbsp;Li Gao ,&nbsp;Zheng Han ,&nbsp;Chen-Xi Feng ,&nbsp;Yang-Ni Li ,&nbsp;Yu-Fei Wang ,&nbsp;Qian Yang ,&nbsp;David K. Simon ,&nbsp;Xue-lian Wang ,&nbsp;Yan Qu ,&nbsp;Bao Wang","doi":"10.1016/j.arr.2025.102995","DOIUrl":"10.1016/j.arr.2025.102995","url":null,"abstract":"<div><div>The accumulation of α-synuclein (α-syn) is a key pathophysiological feature of Parkinson’s disease (PD), and one contributing factor to this aggregation is impaired clearance mechanisms. Recent research has identified the glymphatic system as the brain’s intrinsic waste clearance pathway. This review examines glymphatic dysfunction in PD, with a focus on its impact on α-syn clearance and neurodegeneration. We summarize current evidence showing that disrupted aquaporin-4 (AQP4) polarization, reduced meningeal lymphatic drainage, and sleep disturbances collectively impair glymphatic flow, thereby promoting α-syn aggregation and dopaminergic neuronal loss. We also review emerging neuroimaging approaches, including the Diffusion Tensor Imaging Analysis Along the Perivascular Space (DTI-ALPS) index, enlarged perivascular spaces (EPVSs) and choroid plexus volume (CPV), which increasingly enable in vivo evaluation of glymphatic dysfunction and show correlations with motor severity and cognitive decline. In addition, we discuss potential therapeutic approaches aimed at restoring glymphatic function, including photobiomodulation, pharmacological AQP4 modulation, sleep based interventions, and surgical interventions like deep cervical lymphaticovenular anastomosis (dcLVA). Although these strategies show promise in preclinical studies, their clinical translation remains limited. By integrating insights from glymphatic biology, neuroimaging, and therapeutic development, this review highlights new avenues for PD management and underscores the glymphatic system as a promising therapeutic target for modifying disease progression.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"114 ","pages":"Article 102995"},"PeriodicalIF":12.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145758574","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":"A receptor for glycation end products (RAGE) is a key transmitter between garb-aging and inflammaging","authors":"Zulfiya G. Guvatova ,&nbsp;Anna Vakhrusheva ,&nbsp;Alexey Moskalev","doi":"10.1016/j.arr.2025.102919","DOIUrl":"10.1016/j.arr.2025.102919","url":null,"abstract":"<div><div>A receptor for glycation end products (RAGE) plays a key role in the pathogenesis of many chronic diseases associated with aging. Acting as a multi-ligand sensor, RAGE is able to bind a wide range of stimuli, which fuels inflammation. This makes it a key link between garb-aging and inflammaging. We propose that RAGE functions as the missing molecular link between garb-aging, the progressive buildup of biological waste, and inflammaging, the chronic inflammatory state that drives degenerative disorders. This review summarizes current knowledge on RAGE structure, ligands, and signaling, highlighting its involvement in diabetes, cardiovascular, neurodegenerative, and inflammatory diseases, as well as therapeutic strategies targeting RAGE. By nominating RAGE as a central receptor of garb-aging, we outline new perspectives for combating age-associated pathologies.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"113 ","pages":"Article 102919"},"PeriodicalIF":12.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145310306","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":"In-hospital exercise interventions improve inpatients’ frailty and demonstrate promising implementation outcomes: A systematic review and meta-analysis","authors":"Madeline E. Shivgulam ,&nbsp;Haoxuan Liu ,&nbsp;Zainab Zafar ,&nbsp;Muhammad Cheema ,&nbsp;Shirko Ahmadi ,&nbsp;Olga Theou ,&nbsp;Myles W. O’Brien","doi":"10.1016/j.arr.2025.102934","DOIUrl":"10.1016/j.arr.2025.102934","url":null,"abstract":"<div><h3>Background</h3><div>Frail, hospitalized patients are at a greater risk of further health issues. Frailty levels can worsen during hospitalization, with exercise being one of the best strategies to manage frailty. However, there is a lack of synthesized evidence to indicate whether exercise interventions are effective at managing frailty in this unique setting.</div></div><div><h3>Objective</h3><div>This systematic review and meta-analysis determined if exercise interventions either preserve or improve frailty levels among inpatients.</div></div><div><h3>Methods</h3><div>Sources were searched in May 2024 (updated August 2025) and included Scopus, EMBASE, MEDLINE, CINAHL, and Academic Search Premier. Studies were included if they conducted an exercise intervention in middle-to-older adult (≥45-years) inpatients and assessed frailty as an outcome using any validated frailty assessment tool. The between-group effect size of change in frailty (Intervention vs. Control) was calculated as the standardized mean difference (SMD) using a random effects model.</div></div><div><h3>Results</h3><div>Five studies including n = 810 intervention (age: 82.9 [range: 79–87.6] years; 45 ± 1 % reported females) and 900 control (age: 82.0 [range: 76.0–87.1] years; 44 ± 1 % reported females) participants were included. Improvements in patients’ frailty were observed in n = 3/5 studies. The meta-analysis exhibited a favorable effect on frailty between the intervention and control groups (SMD: 0.716, 95 %CI: 0.119–1.312) with significant heterogeneity between studies (<em>I</em>²=92 %, <em>p</em> &lt; 0.001). No differences were observed between interventions using distinct exercise types or frailty assessment tools (both, <em>p</em> &gt; 0.196)<em>.</em></div></div><div><h3>Conclusion</h3><div>Despite limited available evidence, results indicate exercise training interventions may be effective in improving frailty. This supports the inclusion of exercise interventions beyond usual hospital care to improve frailty.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"113 ","pages":"Article 102934"},"PeriodicalIF":12.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145477377","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":"Reevaluating principal component analysis in geroscience: A call for nonlinear approaches in AI-based evaluations","authors":"Yoshiyasu Takefuji","doi":"10.1016/j.arr.2025.102964","DOIUrl":"10.1016/j.arr.2025.102964","url":null,"abstract":"<div><div>Fuellen et al. (2025) highlighted the essential role of explainable AI methods, particularly principal component analysis (PCA), in evaluating interventions for aging and longevity. However, this paper raises significant concerns regarding PCA's linear and parametric nature, which can misrepresent complex, nonlinear data common in geroscience research. As biological relationships often defy simplistic interpretations, reliance on PCA may obscure vital insights, leading to potential misinterpretations of intervention effects. To enhance accuracy in analyses, this study advocates for the adoption of nonlinear and nonparametric methods, such as Spearman’s rank correlation and Kendall’s tau. By reconsidering their methodological approaches, researchers can foster more accurate and informed evaluations of aging-related interventions.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"113 ","pages":"Article 102964"},"PeriodicalIF":12.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145623651","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":"Contradictory dual role of antinutrients in nutrient inhibition and anti-aging: A comprehensive review on health benefits, processing techniques, and dietary strategies","authors":"Gulsah Karabulut ,&nbsp;Deniz Günal-Köroğlu ,&nbsp;Hilal Yılmaz ,&nbsp;Ezgi Erskine ,&nbsp;Esra Capanoglu","doi":"10.1016/j.arr.2025.102929","DOIUrl":"10.1016/j.arr.2025.102929","url":null,"abstract":"<div><h3>Background</h3><div>Antinutritional factors (antinutrients) are bioactive compounds in plant-derived foods that can impair nutrient absorption and reduce the bioavailability of proteins, carbohydrates, and essential minerals. Major representatives include phytates, oxalates, lectins, tannins, saponins, and enzyme inhibitors, which are associated with adverse nutritional outcomes through interference with nutrient uptake.</div></div><div><h3>Scope and approach</h3><div>Recent studies reveal that antinutrients also possess bioactive properties with potential benefits for aging and longevity. This review assesses their dual role, considering both their inhibitory effects on nutrient utilization and their emerging therapeutic potential, and discusses dietary strategies and processing techniques that minimize risks while enhancing health-promoting properties.</div></div><div><h3>Key findings and conclusions</h3><div>Aging is driven by oxidative stress, inflammation, mitochondrial dysfunction, and cellular senescence, all of which contribute to cancer, cardiovascular disease, and neurodegeneration. Antinutrients may counteract these processes via antioxidant, anti-inflammatory, and autophagy-modulating actions. For instance, phytates protect against oxidative damage, saponins support mitochondrial function, and processing methods such as fermentation, soaking, and germination can reduce harmful effects while preserving bioactivity. Understanding these interactions highlights opportunities to harness antinutrients as functional compounds to promote healthy aging and extend healthspan.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"113 ","pages":"Article 102929"},"PeriodicalIF":12.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145433282","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}