Glia最新文献

{"title":"Regulating the formation of Müller glia-derived progenitor cells in the retina","authors":"Olivia B. Taylor,&nbsp;Heithem M. El-Hodiri,&nbsp;Isabella Palazzo,&nbsp;Levi Todd,&nbsp;Andy J. Fischer","doi":"10.1002/glia.24635","DOIUrl":"10.1002/glia.24635","url":null,"abstract":"<p>We summarize recent findings in different animal models regarding the different cell-signaling pathways and gene networks that influence the reprogramming of Müller glia into proliferating, neurogenic progenitor cells in the retina. Not surprisingly, most of the cell-signaling pathways that guide the proliferation and differentiation of embryonic retinal progenitors also influence the ability of Müller glia to become proliferating Müller glia-derived progenitor cells (MGPCs). Further, the neuronal differentiation of MGPC progeny is potently inhibited by networks of neurogenesis-suppressing genes in chick and mouse models but occurs freely in zebrafish. There are important differences between the model systems, particularly pro-inflammatory signals that are active in mature Müller glia in damaged rodent and chick retinas, but less so in fish retinas. These pro-inflammatory signals are required to initiate the process of reprogramming, but if sustained suppress the potential of Müller glia to become neurogenic MGPCs. Further, there are important differences in how activated Müller glia up- or downregulate pro-glial transcription factors in the different model systems. We review recent findings regarding regulatory cell signaling and gene networks that influence the activation of Müller glia and the transition of these glia into proliferating progenitor cells with neurogenic potential in fish, chick, and mouse model systems.</p>","PeriodicalId":174,"journal":{"name":"Glia","volume":"73 1","pages":"4-24"},"PeriodicalIF":5.4,"publicationDate":"2024-10-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/glia.24635","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142491649","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Long-term reprogramming of primed microglia after moderate inhibition of CSF1R signaling","authors":"Ana León-Rodríguez,&nbsp;Jesús M. Grondona,&nbsp;Sonia Marín-Wong,&nbsp;Manuel F. López-Aranda,&nbsp;María D. López-Ávalos","doi":"10.1002/glia.24627","DOIUrl":"10.1002/glia.24627","url":null,"abstract":"<p>In acute neuroinflammation, microglia activate transiently, and return to a resting state later on. However, they may retain immune memory of such event, namely priming. Primed microglia are more sensitive to new stimuli and develop exacerbated responses, representing a risk factor for neurological disorders with an inflammatory component. Strategies to control the hyperactivation of microglia are, hence, of great interest. The receptor for colony stimulating factor 1 (CSF1R), expressed in myeloid cells, is essential for microglia viability, so its blockade with specific inhibitors (e.g. PLX5622) results in significant depletion of microglial population. Interestingly, upon inhibitor withdrawal, new naïve microglia repopulate the brain. Depletion-repopulation has been proposed as a strategy to reprogram microglia. However, substantial elimination of microglia is inadvisable in human therapy. To overcome such drawback, we aimed to reprogram long-term primed microglia by CSF1R partial inhibition. Microglial priming was induced in mice by acute neuroinflammation, provoked by intracerebroventricular injection of neuraminidase. After 3-weeks recovery, low-dose PLX5622 treatment was administrated for 12 days, followed by a withdrawal period of 7 weeks. Twelve hours before euthanasia, mice received a peripheral lipopolysaccharide (LPS) immune challenge, and the subsequent microglial inflammatory response was evaluated. PLX5622 provoked a 40%–50% decrease in microglial population, but basal levels were restored 7 weeks later. In the brain regions studied, hippocampus and hypothalamus, LPS induced enhanced microgliosis and inflammatory activation in neuraminidase-injected mice, while PLX5622 treatment prevented these changes. Our results suggest that PLX5622 used at low doses reverts microglial priming and, remarkably, prevents broad microglial depletion.</p>","PeriodicalId":174,"journal":{"name":"Glia","volume":"73 1","pages":"175-195"},"PeriodicalIF":5.4,"publicationDate":"2024-10-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/glia.24627","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142491648","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Uptake of alpha-synuclein preformed fibrils is suppressed by inflammation and induces an aberrant phenotype in human microglia","authors":"Jonna Niskanen,&nbsp;Sanni Peltonen,&nbsp;Sohvi Ohtonen,&nbsp;Mohammad Feroze Fazaludeen,&nbsp;Kelvin C. Luk,&nbsp;Luca Giudice,&nbsp;Jari Koistinaho,&nbsp;Tarja Malm,&nbsp;Gundars Goldsteins,&nbsp;Katrina Albert,&nbsp;Šárka Lehtonen","doi":"10.1002/glia.24626","DOIUrl":"10.1002/glia.24626","url":null,"abstract":"<p>Microglia are brain resident immune cells that maintain proteostasis and cellular homeostasis. Recent findings suggest that microglia dysfunction could contribute to the pathogenesis of Parkinson's disease (PD). One of the hallmarks of PD is the aggregation and accumulation of alpha-synuclein (αSyn) into Lewy bodies inside nerve cells. Microglia may worsen the neuronal microenvironment by persistent inflammation, resulting in deficient clearing of aggregated αSyn. To model microglial behavior in PD, we utilized human induced pluripotent stem cells to generate functionally active microglia. We studied the microglial uptake of alpha-synuclein preformed fibrils (PFFs) and the effect of pro-inflammatory stimulation by interferon gamma. We demonstrate that combined exposure disrupts the phagosome maturation pathway while inflammatory stimuli suppress chaperone mediated autophagy and mitochondrial function. Furthermore, inflammatory stimulation impairs PFF uptake in microglia and increases cytokine production. Moreover, excessive PFF uptake by microglia results in induction of inducible nitric oxide synthase. Taken together, we demonstrate that this model is valuable for investigating the behavior of microglia in PD and provide new insights on how human microglia process aggregated αSyn.</p>","PeriodicalId":174,"journal":{"name":"Glia","volume":"73 1","pages":"159-174"},"PeriodicalIF":5.4,"publicationDate":"2024-10-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/glia.24626","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142454222","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Three-dimensional view of microglia—amyloid plaque interactions","authors":"Maria Gotkiewicz,&nbsp;Janne Capra,&nbsp;Pasi O. Miettinen,&nbsp;Teemu Natunen,&nbsp;Heikki Tanila","doi":"10.1002/glia.24628","DOIUrl":"10.1002/glia.24628","url":null,"abstract":"<p>Recent gene expression studies have revealed about 10 different states of microglia, some of which are characteristic for Alzheimer-like amyloid plaque pathology. However, it is not presently known how these translate into morphological features that would reflect microglia interaction with amyloid plaques. With optimized conditions for confocal microscopy in amyloid plaque forming APP/PS1 transgenic mice we reveal new details of how microglia processes interact with amyloid plaques. The microglia contacts differed drastically between purely diffuse plaque and those with a fibrillar core. We identified microglia that extend their enlarged processes through the diffuse shell of the amyloid plaques and cover the fibrillar plaque core with snowplow-like expanded end-feet. These end-feet were filled with the lysosomal marker CD68, while both non-fibrillar and fibrillar amyloid was found in perinuclear vesicles of some “snowplower” microglia. In the organized dense-core plaques, we consistently saw a layer of Apolipoprotein E (ApoE) between the fibrillar core and the microglial end-feet. ApoE covered also loose fibrillar amyloid and diffuse amyloid plaques that were about 10 μm or larger in diameter. These findings are compatible with both amyloid plaque phagocytosis and compaction by microglia. Further, they support a chemotactic role of ApoE for microglia contacts with amyloid plaques.</p>","PeriodicalId":174,"journal":{"name":"Glia","volume":"73 1","pages":"196-209"},"PeriodicalIF":5.4,"publicationDate":"2024-10-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/glia.24628","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142454221","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The antipsychotic chlorpromazine reduces neuroinflammation by inhibiting microglial voltage-gated potassium channels","authors":"Hee-Yoon Lee,&nbsp;Young Lee,&nbsp;Chaelin Chung,&nbsp;Seo-In Park,&nbsp;Hyo Jung Shin,&nbsp;Eun-Hye Joe,&nbsp;Sung Joong Lee,&nbsp;Dong Woon Kim,&nbsp;Su-Hyun Jo,&nbsp;Se-Young Choi","doi":"10.1002/glia.24629","DOIUrl":"10.1002/glia.24629","url":null,"abstract":"<p>Neuroinflammation, the result of microglial activation, is associated with the pathogenesis of a wide range of psychiatric and neurological disorders. Recently, chlorpromazine (CPZ), a dopaminergic D2 receptor antagonist and schizophrenia therapy, was proposed to exert antiinflammatory effects in the central nervous system. Here, we report that the expression of Kv1.3 channel, which is abundant in T cells, is upregulated in microglia upon infection, and that CPZ specifically inhibits these channels to reduce neuroinflammation. In the mouse medial prefrontal cortex, we show that CPZ lessens Kv1.3 channel activity and reduces proinflammatory cytokine production. In mice treated with LPS, we found that CPZ was capable of alleviating both neuroinflammation and depression-like behavior. Our findings suggest that CPZ acts as a microglial Kv1.3 channel inhibitor and neuroinflammation modulator, thereby exerting therapeutic effects in neuroinflammatory psychiatric/neurological disorders.</p>","PeriodicalId":174,"journal":{"name":"Glia","volume":"73 1","pages":"210-227"},"PeriodicalIF":5.4,"publicationDate":"2024-10-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/glia.24629","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142454220","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Molecular profiling of invertebrate glia","authors":"Maria D. Purice,&nbsp;Inês Lago-Baldaia,&nbsp;Vilaiwan M. Fernandes,&nbsp;Aakanksha Singhvi","doi":"10.1002/glia.24623","DOIUrl":"10.1002/glia.24623","url":null,"abstract":"<p><i>Caenorhabditis elegans</i> and <i>Drosophila melanogaster</i> are powerful experimental models for uncovering fundamental tenets of nervous system organization and function. Findings over the last two decades show that molecular and cellular features are broadly conserved between invertebrates and vertebrates, indicating that insights derived from invertebrate models can broadly inform our understanding of glial operating principles across diverse species. In recent years, these model systems have led to exciting discoveries in glial biology and mechanisms of glia–neuron interactions. Here, we summarize studies that have applied current state-of-the-art “-omics” techniques to <i>C. elegans</i> and <i>D. melanogaster</i> glia. Coupled with the remarkable acceleration in the pace of mechanistic studies of glia biology in recent years, these indicate that invertebrate glia also exhibit striking molecular complexity, specificity, and heterogeneity. We provide an overview of these studies and discuss their implications as well as emerging questions where <i>C. elegans</i> and <i>D. melanogaster</i> are well-poised to fill critical knowledge gaps in our understanding of glial biology.</p>","PeriodicalId":174,"journal":{"name":"Glia","volume":"73 3","pages":"632-656"},"PeriodicalIF":5.4,"publicationDate":"2024-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11784859/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142454219","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The role of oligodendrocyte progenitor cells in the spatiotemporal vascularization of the human and mouse neocortex","authors":"Kaiyi Liu,&nbsp;Zhiruo Kang,&nbsp;Min Yang,&nbsp;Fangbing Chen,&nbsp;Mingyang Xia,&nbsp;Wenjuan Dai,&nbsp;Shiyi Zheng,&nbsp;Huiyao Chen,&nbsp;Q. Richard Lu,&nbsp;Wenhao Zhou,&nbsp;Yifeng Lin","doi":"10.1002/glia.24625","DOIUrl":"10.1002/glia.24625","url":null,"abstract":"<p>Brain vasculature formation begins with vessel invasion from the perineural vascular plexus, which expands through vessel sprouting and growth. Recent studies have indicated the existence of oligodendrocyte-vascular crosstalk during development. However, the relationship between oligodendrocyte progenitor cells (OPCs) and the ordered spatiotemporal vascularization of the neocortex has not been elucidated. Our findings suggest that OPCs play a complex role in the vessel density of the embryonic and postnatal neocortex. Analyses of normal human and mouse embryonic cerebral cortex show that vascularization and OPC distribution are tightly controlled in a spatially and temporally restricted manner, exhibiting a positive correlation. Loss of OPCs at both embryonic and postnatal stages led to a reduction in vascular density, suggesting that OPC populations play a role in vascular density. Nonetheless, dynamic observation on cultured brain slices and staining of tissue sections indicate that OPC migration is unassociated with the proximity to blood vessels, primarily occurring along radial glial cell processes. Additionally, <i>in vitro</i> experiments demonstrate that OPC secretions promote vascular endothelial cell (VEC) growth. Together, these observations suggest that vessel density is influenced by OPC secretions.</p>","PeriodicalId":174,"journal":{"name":"Glia","volume":"73 1","pages":"140-158"},"PeriodicalIF":5.4,"publicationDate":"2024-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142398842","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Endogenous histidine peptides are physiological antioxidants that prevent oligodendrocyte cell death and myelin loss in vivo","authors":"Clara Sajrawi,&nbsp;Maali Odeh,&nbsp;Akshay K. Tiwari,&nbsp;Bella Agranovich,&nbsp;Ifat Abramovich,&nbsp;Salman Zubedat,&nbsp;Galit Saar,&nbsp;Lihi Shaulov,&nbsp;Avi Avital,&nbsp;Dan Reznik,&nbsp;Moran Benhar,&nbsp;Inna Radzishevsky,&nbsp;Simone Engelender,&nbsp;Herman Wolosker","doi":"10.1002/glia.24624","DOIUrl":"10.1002/glia.24624","url":null,"abstract":"<p>Histidine dipeptides (HDs) are synthesized in brain oligodendrocytes by carnosine synthase (carns1), but their role is unknown. Using metabolomics and in vivo experiments with both constitutive and oligodendrocyte-selective carns1-KO mouse models, we found that HDs are critical for oligodendrocyte survival and protect against oxidative stress. Carns1-KO mouse models had lower numbers of mature oligodendrocytes, increased lipid peroxidation, and behavioral changes. Cuprizone administration, which increases reactive oxygen species in vivo, resulted in higher oligodendrocyte death, demyelination, axonal alterations, and oxidative damage in the corpus callosum of carns1-KO mice. Gliosis and oxidative damage by cuprizone were prevented by pretreatment with the antioxidant N-acetylcysteine. NADPH levels were increased threefold in the brains of carns1-KO mice as an antioxidant response to oxidative stress through acceleration of the pentose phosphate pathway (PPP). This was due to overexpression of glucose-6-phosphate dehydrogenase, the rate-limiting enzyme of the PPP. Likewise, expression of NAD kinase, the biosynthetic enzyme for NADP+, and NAMPT, which replenishes the NAD+ pool, was higher in carns1-KO mice brains than in controls. Our observations suggest that HDs cell-autonomously protect oligodendrocytes from oxidative stress, with implications for demyelinating diseases.</p>","PeriodicalId":174,"journal":{"name":"Glia","volume":"73 1","pages":"122-139"},"PeriodicalIF":5.4,"publicationDate":"2024-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142363609","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Protein kinase R induced by type I interferons is a main regulator of reactive microglia in Zika virus infection","authors":"Violaine Bortolin,&nbsp;Zeyni Mansuroglu,&nbsp;Laurine Conquet,&nbsp;Gaetano Calcagno,&nbsp;Fanny Lambert,&nbsp;Jose Pablo Marin-Obando,&nbsp;Helena Segrt,&nbsp;Mary Savino,&nbsp;Reyene Menidjel,&nbsp;Sylvie Souès,&nbsp;Luc Buée,&nbsp;Florence Niedergang,&nbsp;Marie-Christine Galas,&nbsp;Xavier Montagutelli,&nbsp;Eliette Bonnefoy","doi":"10.1002/glia.24619","DOIUrl":"10.1002/glia.24619","url":null,"abstract":"<p>Microglial cells are the phagocytic cells of the brain that under physiological conditions participate in brain homeostasis and surveillance. Under pathogenic states, microglia undergoes strong morphological and transcriptional changes potentially leading to sustained neuroinflammation, brain damage, and cognitive disorders. Postnatal and adult Zika virus (ZIKV) brain infection is characterized by the induction of reactive microglia associated with brain inflammation, synapse loss and neuropathogenesis. Contrary to neurons, microglial cells are not infected by ZIKV thus raising the question of the mechanism governing ZIKV-induced microglia's reactivity. In this work, we have questioned the role of exogenous, neuronal type I interferons (IFNs-I) in regulating ZIKV-induced microglia's reactivity. Primary cultured microglial cells were either treated with conditioned media from ZIKV-infected mature neurons or co-cultured with ZIKV-infected neurons. Using either an antibody directed against the IFNAR receptor that neutralizes the IFNs-I response or <i>Ifnar</i>−/−microglial cells, we demonstrate that IFNs-I produced by ZIKV-infected neurons are the main regulators of the phagocytic capacity and the pro-inflammatory gene expression profile of reactive, non-infected microglial cells. We identify protein kinase R (PKR), whose expression is activated by IFNs-I, as a major regulator of the phagocytic capacity, pro-inflammatory response, and morphological changes of microglia induced by IFNs-I while up-regulating STAT1 phosphorylation and IRF1 expression. Results obtained herein in vitro with primary cultured cells and in vivo in ZIKV-infected adult immunocompetent mice, unravel a role for IFNs-I and PKR in directly regulating microglia's reactivity that could be at work in other infectious and non-infectious brain pathologies.</p>","PeriodicalId":174,"journal":{"name":"Glia","volume":"73 1","pages":"80-104"},"PeriodicalIF":5.4,"publicationDate":"2024-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/glia.24619","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142363610","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Developmental maturation and regional heterogeneity but no sexual dimorphism of the murine CNS myelin proteome","authors":"Sophie B. Siems,&nbsp;Vasiliki-Ilya Gargareta,&nbsp;Leonie C. Schadt,&nbsp;Vinicius Daguano Gastaldi,&nbsp;Ramona B. Jung,&nbsp;Lars Piepkorn,&nbsp;Patrizia Casaccia,&nbsp;Ting Sun,&nbsp;Olaf Jahn,&nbsp;Hauke B. Werner","doi":"10.1002/glia.24614","DOIUrl":"10.1002/glia.24614","url":null,"abstract":"<p>The molecules that constitute myelin are critical for the integrity of axon/myelin-units and thus speed and precision of impulse propagation. In the CNS, the protein composition of oligodendrocyte-derived myelin has evolutionarily diverged and differs from that in the PNS. Here, we hypothesized that the CNS myelin proteome also displays variations within the same species. We thus used quantitative mass spectrometry to compare myelin purified from mouse brains at three developmental timepoints, from brains of male and female mice, and from four CNS regions. We find that most structural myelin proteins are of approximately similar abundance across all tested conditions. However, the abundance of multiple other proteins differs markedly over time, implying that the myelin proteome matures between P18 and P75 and then remains relatively constant until at least 6 months of age. Myelin maturation involves a decrease of cytoskeleton-associated proteins involved in sheath growth and wrapping, along with an increase of all subunits of the septin filament that stabilizes mature myelin, and of multiple other proteins which potentially exert protective functions. Among the latter, quinoid dihydropteridine reductase (QDPR) emerges as a highly specific marker for mature oligodendrocytes and myelin. Conversely, female and male mice display essentially similar myelin proteomes. Across the four CNS regions analyzed, we note that spinal cord myelin exhibits a comparatively high abundance of HCN2-channels, required for particularly long sheaths. These findings show that CNS myelination involves developmental maturation of myelin protein composition, and regional differences, but absence of evidence for sexual dimorphism.</p>","PeriodicalId":174,"journal":{"name":"Glia","volume":"73 1","pages":"38-56"},"PeriodicalIF":5.4,"publicationDate":"2024-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/glia.24614","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142337933","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}