Frontiers in Cellular Neuroscience最新文献

{"title":"Corrigendum: Organotypic culture of neonatal murine inner ear explants.","authors":"Jacqueline M Ogier, Rachel A Burt, Hannah R Drury, Rebecca Lim, Bryony A Nayagam","doi":"10.3389/fncel.2024.1512599","DOIUrl":"https://doi.org/10.3389/fncel.2024.1512599","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.3389/fncel.2019.00170.].</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"18 ","pages":"1512599"},"PeriodicalIF":4.2,"publicationDate":"2024-11-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11605511/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142767719","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neuroinflammation modifies the relationship between stress and perivascular spaces in an elderly population with different levels of cognitive impairment.","authors":"Francesca Sibilia, Nasim Sheikh-Bahaei, Wendy J Mack, Giuseppe Barisano, Jeiran Choupan","doi":"10.3389/fncel.2024.1480405","DOIUrl":"10.3389/fncel.2024.1480405","url":null,"abstract":"<p><strong>Background: </strong>Perivascular spaces (PVS) are fluid-filled spaces surrounding the brain parenchymal vasculature. Literature suggests that PVS may play a significant role in aging and neurological disorders, including Alzheimer's disease (AD). The aim of this study is to investigate whether the relationship between MRI-visible PVS and stress is influenced by neuroinflammation in an elderly population with different levels of cognitive impairment.</p><p><strong>Methods: </strong>Using brain MRI scans acquired at 1.5 T, PVS were quantified in a cohort of 461 individuals, consisting of cognitively healthy controls (<i>n</i> = 48), people with mild cognitive impairment (MCI, <i>n</i> = 322) and Alzheimer's disease (AD, <i>n</i> = 91). PVS volume fraction was calculated in the basal ganglia and centrum semiovale using a semi-automated segmentation approach. Stress was quantified with levels of salivary cortisol. Inflammatory biomarkers measured from plasma included cytokines, matrix metalloproteinases and C-reactive protein. General linear models were used to test the relationship between PVS and cortisol, when interacting with inflammatory markers. This was done on the whole cohort and within each clinical cognitive group.</p><p><strong>Results: </strong>In the centrum semiovale, higher inflammation levels reduced the relationship of cortisol with PVS. In basal ganglia, higher levels of C-reactive protein reduced the negative relationship of cortisol with PVS. All analyses were accounted for age, sex, body mass index (BMI) and total hippocampal volume. There was a significant interaction effect between cortisol and C-reactive protein on PVS volume fraction in the MCI group.</p><p><strong>Discussion: </strong>These findings suggest an influence of neuroinflammation on the PVS structure in Alzheimer's disease spectrum, and offer insight for better understanding physiological processes of cognitive impairment onset.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"18 ","pages":"1480405"},"PeriodicalIF":4.2,"publicationDate":"2024-11-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11603360/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142750378","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Transcriptome analyses reveal molecular mechanisms of novel compound heterozygous <i>ACO2</i> variants causing infantile cerebellar retinal degeneration.","authors":"Wenke Yang, Shuyue Wang, Ke Yang, Yanjun Li, Zhenglong Guo, Jianmei Huang, Jinming Wang, Shixiu Liao","doi":"10.3389/fncel.2024.1492048","DOIUrl":"10.3389/fncel.2024.1492048","url":null,"abstract":"<p><strong>Background and purpose: </strong>Infantile cerebellar retinal degeneration (ICRD) (OMIM #614559) is a rare autosomal recessive inherited disease associated with mutations in the aconitase 2 (ACO2) gene. We report a Chinese girl with novel compound heterozygous variants in <i>ACO2</i>, who presented at 7 months of age with psychomotor retardation, truncal hypotonia, and ophthalmologic abnormalities. This study aims to investigate the potential molecular mechanisms underlying <i>ACO2</i> deficiency-induced neuropathy.</p><p><strong>Methods: </strong>Whole exome sequencing was performed on family members to screen for potential pathogenic mutations, followed by Sanger sequencing for validation. Mitochondrial aconitase activity and mitochondrial DNA (mtDNA) copy number were measured using an aconitase activity detection kit and quantitative PCR, respectively. Transcriptome expression profiles from patient cells, and cerebellar and retinal organoids retrieved from the GEO database were integrated. Functional enrichment analysis and protein-protein interaction networks were used to identify key molecules, and their expression levels were validated using Western blot analysis.</p><p><strong>Results: </strong>Genetic testing revealed novel compound heterozygous variations in the proband's <i>ACO2</i> gene (NM:001098), including c.854A>G (p.Asn285Ser) and c.1183C>T (p.Arg395Cys). Predictive analysis of the tertiary structure of the ACO2 protein suggests that both p.Asn285Ser and p.Arg395Cys affect the binding ability of ACO2 to ligands. The mitochondrial aconitase activity and mtDNA copy number in the proband's leukocytes were significantly reduced. Transcriptomic data analysis identified 80 key candidate genes involved in ACO2-related neuropathy. Among these, <i>LRP8</i> and <i>ANK3</i>, whose gene expression levels were significantly positively correlated with <i>ACO2</i>, were further validated by Western blot analysis.</p><p><strong>Conclusions: </strong>This study expands the spectrum of pathogenic <i>ACO2</i> variants, elucidates the potential molecular mechanisms underlying ACO2-related neuropathy, provides in-depth support for the pathogenicity of <i>ACO2</i> genetic variations, and offers new insights into the pathogenesis of ICRD.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"18 ","pages":"1492048"},"PeriodicalIF":4.2,"publicationDate":"2024-11-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11588473/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142727440","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Editorial: Role of ion channels and metabotropic receptors in oligodendrogliogenesis: novel targets for demyelinating pathologies.","authors":"Federica Cherchi, Matthew Swire, Davide Lecca","doi":"10.3389/fncel.2024.1517363","DOIUrl":"10.3389/fncel.2024.1517363","url":null,"abstract":"","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"18 ","pages":"1517363"},"PeriodicalIF":4.2,"publicationDate":"2024-11-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11588474/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142727457","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Does age protect against loss of tonotopy after acute deafness in adulthood?","authors":"Nicole Rosskothen-Kuhl, Sarah Green, Till F Jakob","doi":"10.3389/fncel.2024.1424773","DOIUrl":"10.3389/fncel.2024.1424773","url":null,"abstract":"<p><p>The mammalian auditory system develops a topographical representation of sound frequencies along its pathways, also called tonotopy. In contrast, sensory deprivation during early development results in no or only rudimentary tonotopic organization. This study addresses two questions: (1) How robust is the central tonotopy when hearing fails in adulthood? (2) What role does age play at time of deafness? To address these questions, we deafened young and old adult rats with previously normal hearing. One month after deafening, both groups were unilaterally supplied with cochlear implants and electrically stimulated for 2 h. The central auditory neurons, which were activated as a result of the local electrical intracochlear stimulation, were visualized using Fos staining. While the auditory system of young rats lost the tonotopic organization throughout the brainstem, the auditory system of the older rats mainly sustained its tonotopy. It can be proposed that plasticity prevails in the central auditory system of young adult rats, while network stability prevails in the brains of aging rats. Consequently, age may be an important factor in protecting a hearing-experienced adult auditory system from a rapid loss of tonotopy when suffering from acute hearing loss. Furthermore, the study provides compelling evidence that acute deafness in young adult patients should be diagnosed as early as possible to prevent maladaptation of the central auditory system and thus achieve the optimal hearing outcome with a hearing prosthesis.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"18 ","pages":"1424773"},"PeriodicalIF":4.2,"publicationDate":"2024-11-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11581902/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142709691","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Panaroma of microglia in traumatic brain injury: a bibliometric analysis and visualization study during 2000-2023.","authors":"Yuhang Zhang, Tingzhen Deng, Xiao Ding, Xingyuan Ma, Yatao Wang, Haijun Yang, Ruiwen Ding, Dawen Wang, Haotian Li, Maohua Zheng","doi":"10.3389/fncel.2024.1495542","DOIUrl":"10.3389/fncel.2024.1495542","url":null,"abstract":"<p><strong>Background: </strong>Traumatic brain injury (TBI) is a critical global health concern characterized by elevated rates of both morbidity and mortality. The pathological and physiological changes after TBI are closely related to microglia. Microglia, the primary immune cells in the brain, are closely linked to the mechanisms and treatment of TBI. With increasing research in this area, this study employs bibliometric analysis to identify current research hotspots and predict future trends.</p><p><strong>Objective: </strong>We decided to perform a bibliometric analysis to provide a comprehensive overview of the advancements in microglia research related to traumatic brain injury. We aim to offer researchers insights into current trends and future research directions.</p><p><strong>Method: </strong>We collected all articles and reviews related to microglia and traumatic brain injury published between 2000 and 2023 from the Web of Science Core Collection. These records were analyzed using VOSviewer, CiteSpace, and the R package \"bibliometrix\".</p><p><strong>Results: </strong>We retrieved 665 publications from 25 countries, with the majority contributed by the United States and China. The number of publications on traumatic brain injury and microglia has been steadily increasing each year. Our analysis highlighted the <i>Journal of Neurotrauma</i> and the <i>Journal of Neuroinflammation</i> as the most influential journals in this field. Alan I. Faden and David J. Loane are recognized as leading contributors. Keyword analysis indicates that neuroinflammation, microglial polarization, and neurodegenerative diseases are pivotal areas for future research.</p><p><strong>Conclusion: </strong>In recent years, research on TBI-related microglia has proliferated, with current studies primarily focusing on microglial involvement in neuroinflammation, neurodegenerative changes, and microglial polarization following TBI. Since neuroinflammation and neurodegeneration are two hallmark features of TBI, targeting microglia in TBI treatment may become a central focus for future research.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"18 ","pages":"1495542"},"PeriodicalIF":4.2,"publicationDate":"2024-11-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11578739/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142686394","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Upregulated miR-10b-5p as a potential miRNA signature in amyotrophic lateral sclerosis patients.","authors":"Banaja P Dash, Axel Freischmidt, Anika M Helferich, Albert C Ludolph, Peter M Andersen, Jochen H Weishaupt, Andreas Hermann","doi":"10.3389/fncel.2024.1457704","DOIUrl":"10.3389/fncel.2024.1457704","url":null,"abstract":"<p><p>Amyotrophic lateral sclerosis (ALS) is a fatal, adult-onset disease marked by a progressive degeneration of motor neurons (MNs) present in the spinal cord, brain stem and motor cortex. Death in most patients usually occurs within 2-4 years after symptoms onset. Despite promising progress in delineating underlying mechanisms, such as disturbed proteostasis, DNA/RNA metabolism, splicing or proper nucleocytoplasmic shuttling, there are no effective therapies for the vast majority of cases. A reason for this might be the disease heterogeneity and lack of substantial clinical and molecular biomarkers. The identification and validation of such pathophysiology driven biomarkers could be useful for early diagnosis and treatment stratification. Recent advances in next generation RNA-sequencing approaches have provided important insights to identify key changes of non-coding RNAs (ncRNAs) implicated with ALS disease. Especially, microRNAs (miRNAs) have emerged as key post-transcriptional regulators of gene expression to target several genes/pathways by degrading messenger RNAs (mRNAs) or repressing levels of gene expression. In this study, we expand our previous work to identify top-regulated differentially expressed (DE)-miRNAs by combining different normalizations to search for important and generalisable pathomechanistic dysregulations in ALS as putative novel biomarkers of the disease. For this we performed a consensus pipeline of existing datasets to investigate the transcriptomic profile (mRNAs and miRNAs) of MN cell lines from iPSC-derived <i>SOD1</i>- and <i>TARDBP</i> (TDP-43 protein)-mutant-ALS patients and healthy controls to identify potential signatures and their related pathways associated with neurodegeneration. Transcriptional profiling of miRNA-mRNA interactions from MN cell lines in ALS patients revealed differential expression of genes showed greater vulnerability to KEAP1-NRF2 stress response pathway, sharing a common molecular denominator linked to both disease conditions. We also reported that mutations in above genes led to significant upregulation of the top candidate miR-10b-5p, which we could validate in immortalized lymphoblast cell lines (LCLs) derived from sporadic and familial ALS patients and postmortem tissues of familial ALS patients. Collectively, our findings suggest that miRNA analysis simultaneously performed in various human biological samples may reveal shared miRNA profiles potentially useful as a biomarker of the disease.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"18 ","pages":"1457704"},"PeriodicalIF":4.2,"publicationDate":"2024-11-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11586771/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142715797","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Synaptopodin: a key regulator of Hebbian plasticity.","authors":"Pei You Wu, Yanis Inglebert, R Anne McKinney","doi":"10.3389/fncel.2024.1482844","DOIUrl":"10.3389/fncel.2024.1482844","url":null,"abstract":"<p><p>Synaptopodin, an actin-associated protein found in a subset of dendritic spines in telencephalic neurons, has been described to influence both functional and morphological plasticity under various plasticity paradigms. Synaptopodin is necessary and sufficient for the formation of the spine apparatus, stacks of smooth endoplasmic reticulum cisternae. The spine apparatus is a calcium store that locally regulates calcium dynamics in response to different patterns of activity and is also thought to be a site for local protein synthesis. Synaptopodin is present in ~30% of telencephalic large dendritic spines <i>in vivo</i> and <i>in vitro</i> highlighting the heterogeneous microanatomy and molecular architecture of dendritic spines, an important but not well understood aspect of neuroplasticity. In recent years, it has become increasingly clear that synaptopodin is a formidable regulator of multiple mechanisms essential for learning and memory. In fact, synaptopodin appears to be the decisive factor that determines whether plasticity can occur, acting as a key regulator for synaptic changes. In this review, we summarize the current understanding of synaptopodin's role in various forms of Hebbian synaptic plasticity.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"18 ","pages":"1482844"},"PeriodicalIF":4.2,"publicationDate":"2024-11-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11576213/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142681369","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A sexually dimorphic signature of activity-dependent BDNF signaling on the intrinsic excitability of pyramidal neurons in the prefrontal cortex.","authors":"Kaijie Ma, Daoqi Zhang, Kylee McDaniel, Maria Webb, Samuel S Newton, Francis S Lee, Luye Qin","doi":"10.3389/fncel.2024.1496930","DOIUrl":"10.3389/fncel.2024.1496930","url":null,"abstract":"<p><p>Autism spectrum disorder (ASD) is a group of neurodevelopmental disorders with strong genetic heterogeneity and more prevalent in males than females. We and others hypothesize that diminished activity-dependent neural signaling is a common molecular pathway dysregulated in ASD caused by diverse genetic mutations. Brain-derived neurotrophic factor (BDNF) is a key growth factor mediating activity-dependent neural signaling in the brain. A common single nucleotide polymorphism (SNP) in the pro-domain of the human <i>BDNF</i> gene that leads to a methionine (Met) substitution for valine (Val) at codon 66 (Val66Met) significantly decreases activity-dependent BDNF release without affecting basal BDNF secretion. By using mice with genetic knock-in of this human BDNF methionine (Met) allele, our previous studies have shown differential severity of autism-like social deficits in male and female BDNF^+/Met mice. Pyramidal neurons are the principal neurons in the prefrontal cortex (PFC), a key brain region for social behaviors. Here, we investigated the impact of diminished activity-dependent BDNF signaling on the intrinsic excitability of pyramidal neurons in the PFC. Surprisingly, diminished activity-dependent BDNF signaling significantly increased the intrinsic excitability of pyramidal neurons in male mice, but not in female mice. Notably, significantly decreased thresholds of action potentials were observed in male BDNF^+/Met mice, but not in female BDNF^+/Met mice. Voltage-clamp recordings revealed that the sodium current densities were significantly increased in the pyramidal neurons of male BDNF^+/Met mice, which were mediated by increased transcriptional level of <i>Scn2a</i> encoding sodium channel Na_V 1.2. Medium after hyperpolarization (mAHP), another important parameter to determine intrinsic neuronal excitability, is strongly associated with neuronal firing frequency. Further, the amplitudes of mAHP were significantly decreased in male BDNF^+/Met mice only, which were mediated by the downregulation of <i>Kcnn2</i> encoding small conductance calcium-activated potassium channel 2 (SK2). This study reveals a sexually dimorphic signature of diminished activity-dependent BDNF signaling on the intrinsic neuronal excitability of pyramidal neurons in the PFC, which provides possible cellular and molecular mechanisms underpinning the sex differences in idiopathic ASD patients and human autism victims who carry BDNF Val66Met SNP.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"18 ","pages":"1496930"},"PeriodicalIF":4.2,"publicationDate":"2024-11-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11576208/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142681367","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Outward depolarization of the microglia mitochondrial membrane potential following lipopolysaccharide exposure: a novel screening tool for microglia metabolomics.","authors":"Kendra I McGlothen, Rochelle M Hines, Dustin J Hines","doi":"10.3389/fncel.2024.1430448","DOIUrl":"10.3389/fncel.2024.1430448","url":null,"abstract":"<p><p>Microglia are non-electrogenic immune cells that respond rapidly to protect the central nervous system (CNS) from infections, injuries, or other forms of damage. Microglia mitochondria are essential for providing the requisite energy resources for immune regulation. While fluctuations in energy metabolism are regulated by mitochondria and are reflected in the mitochondrial membrane potential (ΔΨm), there remains a lack of innovation in microglia-centric tools that capitalize on this. In this study, live imaging of microglia in acute slices from EGFP reporter mice expressing EGFP under the control of the fractalkine receptor (CX3CR1) promoter is combined with loading a fluorescent reporter of ΔΨm. Depolarizations in the ΔΨm were recorded after administering the well-characterized immune stimulant lipopolysaccharide (LPS). Microglia ΔΨm increased in distinctive phases with a relatively steep slope following LPS exposure. Conversely, the ΔΨm of neurons showed minimal regulation, highlighting a distinct microglia ΔΨm response to immune stimuli. Analysis of the depolarization of the microglia ΔΨm in the soma, branches, and endfeet revealed progressive changes in each subcellular domain originating in the soma and progressing outward. The inverse agonist emapunil attenuated the depolarization of the ΔΨm across states in a domain-specific manner. These findings emphasize the contribution of mitochondrial membrane dynamics in regulating microglial responses to immune stimuli. Further, this work advances a novel drug screening strategy for the therapeutic regulation of metabolic activity in inflammatory conditions of the brain.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"18 ","pages":"1430448"},"PeriodicalIF":4.2,"publicationDate":"2024-11-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11576292/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142681368","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}