ACS Chemical Neuroscience最新文献

{"title":"Serotonergic System Dysregulation in Alzheimer’s Disease","authors":"Nour F. Al-Ghraiybah,&nbsp;Amer E. Alkhalifa,&nbsp;Dylan Spivey,&nbsp;Thomas Averill,&nbsp;Blake Engelkemier,&nbsp;Patricia Haro Lopez,&nbsp;Mary Grace Stuckey,&nbsp;Luke Jenkins,&nbsp;Amal Kaddoumi","doi":"10.1021/acschemneuro.6c00236","DOIUrl":"10.1021/acschemneuro.6c00236","url":null,"abstract":"<p>Alzheimer’s disease (AD) is a progressive neurodegenerativedisorder characterized by several key hallmarks, including the accumulationof amyloid-β (Aβ), neurofibrillary tangles (NFTs), neuroinflammation,and blood–brain barrier (BBB) dysfunction. Similar to otherneurodegenerative diseases, AD involves disturbances in neurotransmitterhomeostasis. However, the serotonergic system is complex, involvingnumerous mechanisms and pathways, which complicates the establishmentof direct correlations with AD. This review examines the serotonergicsystem, focusing on alterations in serotonin (5-HT), its transporter,and its receptors in the context of AD, to identify current knowledgegaps and highlight ongoing research directions. It also emphasizesthe role of 5-HT in vascular regulation and BBB integrity, and linksthe gut-brain axis to the serotonergic system.</p>","PeriodicalId":13,"journal":{"name":"ACS Chemical Neuroscience","volume":"17 15","pages":"2843–2857"},"PeriodicalIF":4.5,"publicationDate":"2026-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148443470","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":"Microbes and Microbial Chemical Matter in the Seeding of Alzheimer’s Disease: Prospects for Orthogonal Therapies","authors":"Naveen Kumar,&nbsp;Venkateswarlu Yarlagadda","doi":"10.1021/acschemneuro.6c00255","DOIUrl":"10.1021/acschemneuro.6c00255","url":null,"abstract":"<p>Alzheimer’s disease (AD) remains the leading causeof dementia,with mortality rates having doubled over the past two to three decadesand projected to rise with continued population aging. Despite itsprofound health and economic impact, effective therapeutic and preventiveinterventions remain limited, largely owing to an incomplete understandingof its etiopathogenesis. Emerging evidence indicates that microbes,including viruses, bacteria, and fungi, as well as their associatedmetabolites, toxins, and structural components, are involved in thedevelopment of AD. Microbial invasion, through dysbiosis or infection,can trigger neuroinflammation that drives overproduction of amyloidβ peptide (AβP). AβP functions as a broad-spectrumantimicrobial agent, and its accumulation, a key pathological hallmarkof AD, is promoted by microbial presence as part of the immune response.Maintaining microbial eubiosis, preventing infections that impactthe nervous system (e.g., herpes zoster), supporting gut microbiomehomeostasis through prebiotics, and the judicious use of antimicrobialinterventions may mitigate AD onset and progression. This Review delineatesthe involvement of microbes and their components in the initiationof AD and presents the prospects of orthogonal therapies to controlAD.</p>","PeriodicalId":13,"journal":{"name":"ACS Chemical Neuroscience","volume":"17 15","pages":"2858–2879"},"PeriodicalIF":4.5,"publicationDate":"2026-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148534594","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":"Decreased Sphingosine 1-Phosphate Levels in the Prefrontal Cortex of Mice Susceptible to Repeated Social Defeat Stress","authors":"Katsuya Morito,&nbsp;Suzumi Kimura,&nbsp;Saki Fujisawa,&nbsp;Yuki Nishimura,&nbsp;Kentaro Takayama","doi":"10.1021/acschemneuro.6c00163","DOIUrl":"10.1021/acschemneuro.6c00163","url":null,"abstract":"<p>Repeated psychological stress is a major risk factorfor psychiatricdisorders. Sphingosine 1-phosphate (S1P), a bioactive sphingolipid,is known to contribute to regulating central nervous system functions.However, the relationship between the onset of psychological stress-inducedbehavioral disorders and S1P metabolism in the brain remains poorlyunderstood. Because prefrontal cortex (PFC) and hippocampus are keybrain regions involved in psychological stress responses, we investigatedwhether repeated social defeat stress (SDS) alters S1P metabolismin these regions. The S1P levels in the PFC, but not in the hippocampus,of mice susceptible to 4-day SDS were markedly lower than those inthe control mice and were positively correlated with sociability.Additionally, mRNA expressions of an S1P-degrading enzyme <em>Plpp3</em> and an inflammatory mediator <em>Hmgb1</em> were increased in the PFC of 4-day SDS-susceptible mice. These resultssuggest that impaired S1P signaling in the PFC is associated withthe onset of psychosocial stress-induced social avoidance.</p>","PeriodicalId":13,"journal":{"name":"ACS Chemical Neuroscience","volume":"17 15","pages":"2893–2900"},"PeriodicalIF":4.5,"publicationDate":"2026-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148546984","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":"Role of β-Arrestin2 Signaling in Neuropharmacological Effects of Psychedelic Drugs","authors":"Aurelija Ippolito,&nbsp;Agnese Tiranti,&nbsp;Shaun Hurley,&nbsp;Gary Gilmour,&nbsp;Grant Churchill,&nbsp;Trevor Sharp","doi":"10.1021/acschemneuro.6c00138","DOIUrl":"10.1021/acschemneuro.6c00138","url":null,"abstract":"<p>Current research into the actions of psychedelic drugsis focusedon 5-HT_2A receptor-coupled signaling pathways, particularlyβ-arrestin2 signaling. Here, we investigated the involvementof β-arrestin2 in psychedelic drug-induced mouse markers ofhallucinogenic effects, molecular plasticity, and structural plasticity;specifically, the head-twitch response, cortical expression of plasticity-relatedgenes (<em>cFos</em>, <em>Egr1</em>, <em>Egr2</em>, and <em>Arc</em>), and dendritogenesis (primary corticalneuron cultures), respectively. Psilocin-induced head-twitches, plasticitygene expression, and dendritogenesis were all blocked by the 5-HT_2A receptor antagonist MDL-100,907. The head-twitch responseto psilocin was not different between wildtype and β-arrestin2knockout (KO) mice, and the head-twitch responses to 2,5-dimethoxy-4-iodoamphetamine(DOI) and lysergic acid diethylamide (LSD) were similarly unaffectedby β-arrestin2 KO. Psilocin-evoked gene expression showed atrend to be less in β-arrestin2 KO compared to wildtype mice,but the gene expression response to DOI was clearly not altered byβ-arrestin2 KO. Finally, psilocin-induced dendritogenesis wasattenuated in β-arrestin2 KO versus wild-type cultured neurons,and similar findings were obtained with DOI. In summary, the currentstudy found no convincing evidence to support a role for β-arrestin2signaling in either the head-twitch or plasticity-related gene responsesto the psychedelic drugs tested. However, our data suggest a rolefor the β-arrestin2 pathway in psychedelic drug-evoked dendritogenesisof cultured neurons. Thus, the β-arrestin2 pathway unlikelymediates the hallucinogenic effects of psychedelic drugs but may contributeto neural plasticity changes in certain models.</p>","PeriodicalId":13,"journal":{"name":"ACS Chemical Neuroscience","volume":"17 15","pages":"2971–2981"},"PeriodicalIF":4.5,"publicationDate":"2026-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148676127","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":"Elevation of Beta-2 Microglobulin during Prion Infection is Closely Correlated with PrPSc Accumulation and is Independent of MHC-I","authors":"Xiao-Xi Jia,&nbsp;Bing Xu,&nbsp;Chao Hu,&nbsp;Ru-Han A,&nbsp;Wei-Wei Zhang,&nbsp;Li-Ping Gao,&nbsp;Kang Xiao,&nbsp;Qi Shi,&nbsp;Cao Chen,&nbsp;Xiao-Ping Dong","doi":"10.1021/acschemneuro.5c00911","DOIUrl":"10.1021/acschemneuro.5c00911","url":null,"abstract":"<p>β2-microglobulin (B2M) is implicatedin neuroinflammatoryand neurodegenerative processes, but its role in prion diseases remainsunclear. Here, the alterations in B2M expression and distributionas well as its correlation with PrP^Sc accumulation wereinvestigated in several scrapie-infected rodent models and a prion-infectedcell line. Markedly increased B2M levels were detected in the brainsof prion-infected rodents at the terminal stage, as well as in theprion-infected SMB-S15 cells, with prominent colocalization with neuronsand microglia. Transient overexpression of cytosolic abnormal PrPin cultured cells induced an increase in B2M, whereas the expressionof wild-type PrP did not alter the B2M level. Resveratrol-inducedclearance of PrP^Sc in SMB-S15 cells sufficiently reversedthe increased level of B2M. Molecular interactions and histologicalspatial distributions between B2M and PrP^Sc were identifiedin scrapie-infected brains. The B2M upregulation during prion infectionwas independent of the MHC-I expression. Routine Western blot andELISA failed to find significant differences in B2M levels betweenthe cohorts of human prion disease (PrD) and non-PrD in cerebrospinalfluid (CSF), and between the cohorts of PrD and the normal populationin serum. These findings suggest that prion infection and abnormalPrP accumulation induce remarkable B2M upregulation, and this interactionalong with its MHC-I-independent upregulation highlights the potentialof B2M in the pathological progression of prion diseases, providinga novel molecular basis for understanding prion-induced neuroinflammation.</p>","PeriodicalId":13,"journal":{"name":"ACS Chemical Neuroscience","volume":"17 15","pages":"2918–2932"},"PeriodicalIF":4.5,"publicationDate":"2026-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148429340","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":"Emerging Promise of Sulforaphane in Autism: A Comprehensive Review of Its Therapeutic Potential and Mechanisms","authors":"Xinming Zhang,&nbsp;Qi He,&nbsp;Yuan yuan Zhu,&nbsp;George H. Lorimer,&nbsp;Hasan Bayram,&nbsp;Reza A. Ghiladi,&nbsp;Jun Wang","doi":"10.1021/acschemneuro.6c00282","DOIUrl":"10.1021/acschemneuro.6c00282","url":null,"abstract":"<p>Autism spectrum disorder (ASD) is a complex neurodevelopmentaldisorder that emerges in early childhood and significantly impactsthe quality of life for individuals and families. Currently, thereare no specific medications available for ASD. Increasing attentionis now focused on bioactive compounds with anti-inflammatory and antioxidantproperties. Sulforaphane (SFN), a key member of the isothiocyanatefamily, is abundant in cruciferous vegetables. It exhibits potentantioxidant and anti-inflammatory effects with minimal side effects,while oxidative stress and inflammation are recognized triggers inASD pathogenesis. As research deepens, SFN’s physiologicalactivities─including antioxidant, neuroprotective, and anti-inflammatoryproperties are gaining heightened attention. Building on prior studies,this review comprehensively summarizes seven potential pathways throughwhich SFN protects neurodevelopment or reverses ASD-related neuraldamage, including Keap1/Nrf2/ARE; MAPKs; NF-κB; HSR; AhR/CYP1;Sirtuin-FOXO; and mTOR/autophagy signaling pathways, elucidating thepotential mechanisms underlying its multifaceted actions. This reviewoffers new insights for the comprehensive utilization of sulforaphaneand the treatment of ASD.</p>","PeriodicalId":13,"journal":{"name":"ACS Chemical Neuroscience","volume":"17 15","pages":"2880–2892"},"PeriodicalIF":4.5,"publicationDate":"2026-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148519599","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":"5-HT4 Receptor Ligand RS67333 Modulates Striatal Acetylcholine and Dopamine Release via the Inhibition of Acetylcholinesterase","authors":"Qinbo Qiao,&nbsp;Wenhui Wu,&nbsp;Stephanie J. Cragg","doi":"10.1021/acschemneuro.6c00342","DOIUrl":"10.1021/acschemneuro.6c00342","url":null,"abstract":"<p>Serotonin 5-HT4 receptors (5-HT₄Rs) have emergedaspotential therapeutic targets in neuropsychiatric and neurodegenerativedisorders by modulating circuits that shape mood, cognition, and motorfunctions. Ligands for 5-HT₄Rs can modify dopamine (DA)and acetylcholine (ACh) transmission, but mechanisms and circuitshave not been fully resolved. Some 5-HT₄R agonists havebeen suggested to have effects that include the inhibition of acetylcholinesterase(AChE), raising the speculation that 5-HT₄R ligands mightmodulate ACh and DA through this action. Here, we investigated theimpact of RS67333, a partial 5-HT₄R agonist, on DA andACh release dynamics in the striatum detected <em>ex vivo</em> in mouse brain slices using fast-scan cyclic voltammetry (FCV) andgenetically encoded ACh sensor GRAB_ACh3.0, respectively.We found that RS67333 significantly modulated electrically evokedDA release in the dorsolateral striatum (DLS) and nucleus accumbenscore, effects that were abolished by a nicotinic receptor (nAChR)antagonist. In parallel, RS67333 altered evoked ACh signals by extendingextracellular ACh lifetime, and correspondingly, RS67333 was foundto inhibit striatal AChE enzymatic activity. By contrast, BIMU8, analternative 5-HT₄R ligand that did not inhibit striatalAChE, had no effect on the evoked striatal ACh or DA release. Thesefindings indicate that RS67333 modulates striatal ACh transmission,which shapes downstream regulation of DA release by nAChRs, not through5-HT₄Rs but through AChE inhibition. These findings emphasizethe caution due in attributing functions to 5-HT₄Rs butalso highlight an alternative pharmacological profile of some purported5-HT₄R ligands as AChE inhibitors of potential utilityfor treating ACh/DA disorders.</p>","PeriodicalId":13,"journal":{"name":"ACS Chemical Neuroscience","volume":"17 15","pages":"3013–3022"},"PeriodicalIF":4.5,"publicationDate":"2026-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148534608","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":"Single-Cell Proteomics Reveals Proteome Remodeling and Cellular Heterogeneity During NGF-Induced PC12 Neuronal Differentiation","authors":"Arpa Ebrahimi,&nbsp;Shuxin Chi,&nbsp;Jun Yang,&nbsp;Phoebe Y. Lee,&nbsp;Prongbaramee K. Colling,&nbsp;Hailey Mendenhall,&nbsp;Chad Giusti,&nbsp;David A. Hendrix,&nbsp;Leonard J. Foster,&nbsp;Claudia S. Maier","doi":"10.1021/acschemneuro.6c00109","DOIUrl":"10.1021/acschemneuro.6c00109","url":null,"abstract":"<p>Single-cell proteomicsenables direct measurement of cellular heterogeneityduring dynamic biological processes, but its application to fragileand highly adherent neuronal models remains challenging. Here, wedeveloped and applied an optimized single-cell proteomics workflowto characterize proteome remodeling during nerve growth factor (NGF)-induceddifferentiation of PC12 cells. To enable reliable single-cell analysis,we implemented gentle dissociation, antiaggregation strategies, andthermal inkjet-based cell dispensing, achieving high accuracy in single-cellisolation. Inclusion of <em>n</em>-dodecyl-β-<span>d</span>-maltoside (DDM) improved recovery of membrane-associated and low-solubilityproteins. Coupled with LC–ion mobility–mass spectrometry,this workflow enabled quantification of 2,000–3,000 proteinsper cell across the differentiation time course. Single-cell proteomicanalysis revealed progressive and heterogeneous proteome remodelingduring differentiation. While undifferentiated cells formed a relativelyhomogeneous population, later stages (Days 4–6) exhibited increasedvariability, including multimodal protein abundance distributionsand separation into distinct subpopulations. Dimensionality reduction,clustering, and non-negative matrix factorization identified multiplecoexisting proteomic states within the same time points, reflectingasynchronous differentiation trajectories. These subpopulations werecharacterized by coordinated differences in pathways related to intracellulartrafficking, protein translation, cytoskeletal organization, and neuronalmaturation. Comparison with bulk proteomics demonstrated that proteinsassociated with differentiated neuronal states, including those involvedin neurite formation and structural remodeling, are underrepresentedin population-averaged measurements but are enriched within specificsingle-cell subpopulations. Temporal and cluster-resolved analysesfurther revealed distinct protein expression trajectories, includingearly decreases in cell cycle and metabolic pathways and later increasesin neuronal structural and regulatory proteins. Together, this studyestablishes an optimized workflow for single-cell proteomics of neuronalsystems and demonstrates that NGF-induced PC12 differentiation proceedsthrough heterogeneous and divergent proteomic states that are notresolved by bulk analysis.</p>","PeriodicalId":13,"journal":{"name":"ACS Chemical Neuroscience","volume":"17 15","pages":"2933–2948"},"PeriodicalIF":4.5,"publicationDate":"2026-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148676216","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":"Modulating Stress Granules via HDAC6 Inhibition: A Promising Strategy against Alzheimer’s Disease","authors":"Emona Jagaselvan,&nbsp;Prasenjit Mondal,&nbsp;Can Zhang","doi":"10.1021/acschemneuro.6c00264","DOIUrl":"10.1021/acschemneuro.6c00264","url":null,"abstract":"<p>Emergingevidence suggests that dysregulated cellularstress responses,particularly the formation and persistence of stress granules (SGs),may significantly contribute to Alzheimer’s disease (AD) pathogenesis.SGs are dynamic, membrane-less ribonucleoprotein assemblies that sequesterstalled translation preinitiation complexes during cellular stress.Under physiological conditions, SGs are transient and disassembleupon stress resolution, often facilitated by heat shock proteins (HSPs).However, under chronic stress, persistent or aberrant SGs can form,which may seed pathological protein aggregation and exacerbate proteostaticimbalance, neuroinflammation, and neurodegeneration. Despite the growingbody of evidence linking HDAC6 to SG dynamics and AD pathology, theprecise mechanistic relationship remains unresolved. This review highlightsthe current understanding of HDAC6-mediated SG regulation in AD, identifiescritical knowledge gaps, and discusses the therapeutic potential ofselective HDAC6 inhibition in modulating SG pathology and neuroinflammation.</p>","PeriodicalId":13,"journal":{"name":"ACS Chemical Neuroscience","volume":"17 15","pages":"2771–2774"},"PeriodicalIF":4.5,"publicationDate":"2026-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148589246","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":"PTEN Negatively Regulates Spastin Ser210 Phosphorylation To Modulate GluA1 Surface Trafficking and Excitatory Synaptic Transmission","authors":"Danlei Liu,&nbsp;Jiagui Zhong,&nbsp;Laijian Wang,&nbsp;Xiaonan Zhu,&nbsp;Shubin Chen,&nbsp;Jiong Li,&nbsp;Guoqing Guo,&nbsp;Caihui Cha,&nbsp;Jifeng Zhang,&nbsp;Guangyin Yu,&nbsp;Yuchuan Zhong","doi":"10.1021/acschemneuro.6c00114","DOIUrl":"10.1021/acschemneuro.6c00114","url":null,"abstract":"<p>Asa key component of the cytoskeleton, microtubule dynamics providestructural support for neurite growth. Spastin plays a critical rolein reshaping microtubule arrangement, which is essential for axondevelopment and regeneration. However, the mechanism by which spastinis activated and functions remains unclear. In this study, we discoveredthat phosphorylation of spastin at Ser210 promotes dendrite growthand surface expression of GluA1 in neurons, enhancing synaptic transmission.Conversely, dephosphorylation of spastin inhibits dendrite growthand surface expression of GluA1, weakening synaptic transmission.PTEN interacts with the MIT domain of spastin through its C-terminalregion, resulting in reduced spastin phosphorylation expression levels.This process suppresses the transport of the AMPA receptor GluA1 subunit,thereby modulating neurite outgrowth and weakening synaptic transmission.In conclusion, our research indicates that PTEN is the pathway thatregulates the phosphorylation of spastin, providing an important referencefor the treatment of neurological diseases characterized by microtubuledysregulation.</p>","PeriodicalId":13,"journal":{"name":"ACS Chemical Neuroscience","volume":"17 15","pages":"2949–2960"},"PeriodicalIF":4.5,"publicationDate":"2026-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148467775","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}