Glia最新文献

{"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}

{"title":"The role of ATP citrate lyase in myelin formation and maintenance","authors":"Andrew Schneider,&nbsp;Seongsik Won,&nbsp;Eric A. Armstrong,&nbsp;Aaron J. Cooper,&nbsp;Amulya Suresh,&nbsp;Rachell Rivera,&nbsp;Gregory Barrett-Wilt,&nbsp;John M. Denu,&nbsp;Judith A. Simcox,&nbsp;John Svaren","doi":"10.1002/glia.24620","DOIUrl":"10.1002/glia.24620","url":null,"abstract":"<p>Formation of myelin by Schwann cells is tightly coupled to peripheral nervous system development and is important for neuronal function and long-term maintenance. Perturbation of myelin causes a number of specific disorders that are among the most prevalent diseases affecting the nervous system. Schwann cells synthesize myelin lipids de novo rather than relying on uptake of circulating lipids, yet one unresolved matter is how acetyl CoA, a central metabolite in lipid formation is generated during myelin formation and maintenance. Recent studies have shown that glucose-derived acetyl CoA itself is not required for myelination. However, the importance of mitochondrially-derived acetyl CoA has never been tested for myelination in vivo. Therefore, we have developed a Schwann cell-specific knockout of the ATP citrate lyase (<i>Acly</i>) gene to determine the importance of mitochondrial metabolism to supply acetyl CoA in nerve development. Intriguingly, the ACLY pathway is important for myelin maintenance rather than myelin formation. In addition, ACLY is required to maintain expression of a myelin-associated gene program and to inhibit activation of the latent Schwann cell injury program.</p>","PeriodicalId":174,"journal":{"name":"Glia","volume":"73 1","pages":"105-121"},"PeriodicalIF":5.4,"publicationDate":"2024-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/glia.24620","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142337934","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":"Towards an integrated approach for understanding glia in Amyotrophic Lateral Sclerosis","authors":"Stanislaw Majewski,&nbsp;Pierre Klein,&nbsp;Séverine Boillée,&nbsp;Benjamin E. Clarke,&nbsp;Rickie Patani","doi":"10.1002/glia.24622","DOIUrl":"10.1002/glia.24622","url":null,"abstract":"<p>Substantial advances in technology are permitting a high resolution understanding of the salience of glia, and have helped us to transcend decades of predominantly neuron-centric research. In particular, recent advances in ‘omic’ technologies have enabled unique insights into glial biology, shedding light on the cellular and molecular aspects of neurodegenerative diseases, including amyotrophic lateral sclerosis (ALS). Here, we review studies using omic techniques to attempt to understand the role of glia in ALS across different model systems and post mortem tissue. We also address caveats that should be considered when interpreting such studies, and how some of these may be mitigated through either using a multi-omic approach and/or careful low throughput, high fidelity orthogonal validation with particular emphasis on functional validation. Finally, we consider emerging technologies and their potential relevance in deepening our understanding of glia in ALS.</p>","PeriodicalId":174,"journal":{"name":"Glia","volume":"73 3","pages":"591-607"},"PeriodicalIF":5.4,"publicationDate":"2024-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11784848/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142337935","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":"Aberrant neurodevelopment in human iPS cell-derived models of Alexander disease","authors":"Zuzana Matusova,&nbsp;Werner Dykstra,&nbsp;Yolanda de Pablo,&nbsp;Oskar G. Zetterdahl,&nbsp;Isaac Canals,&nbsp;Charlotte A. G. H. van Gelder,&nbsp;Harmjan R. Vos,&nbsp;Dolores Pérez-Sala,&nbsp;Mikael Kubista,&nbsp;Pavel Abaffy,&nbsp;Henrik Ahlenius,&nbsp;Lukas Valihrach,&nbsp;Elly M. Hol,&nbsp;Milos Pekny","doi":"10.1002/glia.24618","DOIUrl":"10.1002/glia.24618","url":null,"abstract":"<p>Alexander disease (AxD) is a rare and severe neurodegenerative disorder caused by mutations in glial fibrillary acidic protein (GFAP). While the exact disease mechanism remains unknown, previous studies suggest that mutant GFAP influences many cellular processes, including cytoskeleton stability, mechanosensing, metabolism, and proteasome function. While most studies have primarily focused on GFAP-expressing astrocytes, GFAP is also expressed by radial glia and neural progenitor cells, prompting questions about the impact of GFAP mutations on central nervous system (CNS) development. In this study, we observed impaired differentiation of astrocytes and neurons in co-cultures of astrocytes and neurons, as well as in neural organoids, both generated from AxD patient-derived induced pluripotent stem (iPS) cells with a GFAP^R239C mutation. Leveraging single-cell RNA sequencing (scRNA-seq), we identified distinct cell populations and transcriptomic differences between the mutant GFAP cultures and a corrected isogenic control. These findings were supported by results obtained with immunocytochemistry and proteomics. In co-cultures, the GFAP^R239C mutation resulted in an increased abundance of immature cells, while in unguided neural organoids and cortical organoids, we observed altered lineage commitment and reduced abundance of astrocytes. Gene expression analysis revealed increased stress susceptibility, cytoskeletal abnormalities, and altered extracellular matrix and cell–cell communication patterns in the AxD cultures, which also exhibited higher cell death after stress. Overall, our results point to altered cell differentiation in AxD patient-derived iPS-cell models, opening new avenues for AxD research.</p>","PeriodicalId":174,"journal":{"name":"Glia","volume":"73 1","pages":"57-79"},"PeriodicalIF":5.4,"publicationDate":"2024-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/glia.24618","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142277637","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":"Are we there yet? Exploring astrocyte heterogeneity one cell at a time","authors":"Michael R. O'Dea,&nbsp;Philip Hasel","doi":"10.1002/glia.24621","DOIUrl":"10.1002/glia.24621","url":null,"abstract":"<p>Astrocytes are a highly abundant cell type in the brain and spinal cord. Like neurons, astrocytes can be molecularly and functionally distinct to fulfill specialized roles. Recent technical advances in sequencing-based single cell assays have driven an explosion of omics data characterizing astrocytes in the healthy, aged, injured, and diseased central nervous system. In this review, we will discuss recent studies which have furthered our understanding of astrocyte biology and heterogeneity, as well as discuss the limitations and challenges of sequencing-based single cell and spatial genomics methods and their potential future utility.</p>","PeriodicalId":174,"journal":{"name":"Glia","volume":"73 3","pages":"619-631"},"PeriodicalIF":5.4,"publicationDate":"2024-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11784854/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142277638","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":"Leptin reduces LPS-induced A1 reactive astrocyte activation and inflammation via inhibiting p38-MAPK signaling pathway","authors":"Meiqi Sun,&nbsp;Yiqun Song,&nbsp;Xiaoxuan Hu,&nbsp;Zixuan Zhang,&nbsp;Ruolan Tan,&nbsp;Zhenlu Cai,&nbsp;Xinyi Wang,&nbsp;Yali Fu,&nbsp;Hongli You,&nbsp;Simeng Cui,&nbsp;Wanting Zhao,&nbsp;Jing An,&nbsp;Xinlin Chen,&nbsp;Haixia Lu","doi":"10.1002/glia.24611","DOIUrl":"10.1002/glia.24611","url":null,"abstract":"<p>Neurotoxic A1 reactive astrocytes are induced by inflammatory stimuli. Leptin has been confirmed to have neuroprotective properties. However, its effect on the activation of A1 astrocytes in infectious inflammation is unclear. In the current study, astrocytes cultured from postnatal day 1 Sprague–Dawley rats were stimulated with lipopolysaccharide (LPS) to induce an acute in vitro inflammatory response. Leptin was applied 6 h later to observe its protective effects. The viability of the astrocytes was assessed. A1 astrocyte activation was determined by analyzing the gene expression of <i>C3</i>, <i>H2-D1</i>, <i>H2-T23</i>, and <i>Serping 1</i> and secretion of pro-inflammatory cytokines IL-6 and TNF-α. The levels of phospho-p38 (pp38) and nuclear factor-κB (NF-κB) phosphor-p65 (pp65) were measured to explore the possible signaling pathways. Additionally, an LPS-induced inflammatory animal model was established to investigate the in vivo effects of leptin on A1 astrocytic activation. Results showed that in the in vitro culture system, LPS stimulation caused elevated expression of A1 astrocyte-specific genes and the secretion of pro-inflammatory cytokines, indicating the activation of A1 astrocytes. Leptin treatment significantly reversed the LPS induced upregulation in a dose-dependent manner. Similarly, LPS upregulated pp38, NF-κB pp65 protein and inflammatory cytokines were successfully reduced by leptin. In the LPS-induced animal model, the amelioratory effect of leptin on A1 astrocyte activation and inflammation was further confirmed, showed by the reduced sickness behaviors, A1 astrocyte genesis and inflammatory cytokines in vivo. Our results demonstrate that leptin efficiently inhibits LPS-induced neurotoxic activation of A1 astrocytes and neuroinflammation by suppressing p38-MAPK signaling pathway.</p>","PeriodicalId":174,"journal":{"name":"Glia","volume":"73 1","pages":"25-37"},"PeriodicalIF":5.4,"publicationDate":"2024-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142277648","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":"Microglial morphology aligns with vigilance stage-specific neuronal oscillations in a brain region-dependent manner","authors":"Sarah Steffens,&nbsp;Hilla Mäkinen,&nbsp;Tarja Stenberg,&nbsp;Henna-Kaisa Wigren","doi":"10.1002/glia.24617","DOIUrl":"10.1002/glia.24617","url":null,"abstract":"<p>Microglia, the resident immune cells in the brain, dynamically adapt their morphology based on their functional state. This study explored the relationship between microglial morphology and sleep–wake cycles in mice. Using Iba1 immunostaining to identify microglia, we quantified morphological changes in microglia at different timepoints in multiple brain regions (cortex, hippocampus, basal forebrain, hindbrain, and cerebellum) in B6 male mice using semi-automated 3D structural analysis. Simultaneously, in a separate group, we monitored wake and sleep stage-specific brain activity using EEG/EMG recordings. During natural sleep–wake cycles, we observed increased microglial complexity (enlarged volume, territorial coverage, and ramification) during wakefulness, characterized by high-frequency theta (8–12 Hz) and gamma activity (30–80 Hz). Conversely, during NREM sleep, which is dominated by delta activity (0.5–4 Hz), microglia displayed reduced complexity. Notably, this pattern was absent in brain regions lacking direct functional connections to areas generating vigilance stage-dependent thalamocortical oscillations. We then extended wakefulness to decouple circadian influence from sleep–wake-specific neuronal activity. This procedure attenuated the decrease in microglial complexity observed during natural sleep, suggesting a crucial role for neuronal activity. Subsequent recovery sleep restored microglial features, independent of the time of day (zeitgeber time). These findings reveal a dynamic interplay between vigilance stage-specific thalamocortical activity and microglial morphology across various brain regions. This suggests a potential role for microglia in sleep regulation and warrants further investigation to understand the underlying mechanisms.</p>","PeriodicalId":174,"journal":{"name":"Glia","volume":"72 12","pages":"2344-2356"},"PeriodicalIF":5.4,"publicationDate":"2024-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/glia.24617","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142277649","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}