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1,360 results for “Microglia”
Pro-inflammatory activation of primary microglia and macrophages increases 18kDa Translocator Protein (TSPO) expression in rodents but not humans
<p>Data underpinning JCBFM paper entitled: Pro-inflammatory activation of primary microglia and macrophages increases 18kDa Translocator Protein (TSPO) expression in rodents but not humans</p>
Morphological parameters of microglia in the CDS-based microglia depletion model
<p>The data set includes morphological parameters (cell soma size, process length, branching points, and Sholl analysis) of microglial cells after treatment with clodronate disodium salt (CDS), phosphate buffered saline (PBS) or sham in mice.</p>
Rapid phagosome isolation enables unbiased multiomic analysis of human microglia phagosomes 4
<p>Metabolomic data from phagosomes, controls and whole cell fractions of human ex vivo microglia.</p>
Immune responses in mice lacking STAT-1 in microglia
<p><em>Toxoplasma gondii</em> is a ubiquitous intracellular protozoan parasite that establishes a life-long chronic infection largely restricted to the central nervous system (CNS). Constant immune pressure, notably IFN-γ-STAT1 signaling, is required for preventing fatal pathology during <em>T. gondii</em> infection. Here, we report that abrogation of STAT1 signaling in microglia, the resident immune cells of the CNS, is sufficient to induce a loss of parasite control in the CNS and susceptibility to toxoplasmic encephalitis during the early stages of chronic infection. Using a microglia-specific genetic labeling and targeting system that discriminates microglia from blood-derived myeloid cells that infiltrate the brain during infection, we find that, contrary to previous in vitro reports, microglia do not express inducible nitric-oxide synthase (iNOS) during <em>T. gondii</em> infection in vivo. Instead, transcriptomic analyses of microglia reveal that STAT1 regulates both (i) a transcriptional shift from homeostatic to "disease-associated microglia" (DAM) phenotype conserved across several neuroinflammatory models, including <em>T. gondii</em> infection, and (ii) the expression of anti-parasitic cytosolic molecules that are required for eliminating T. gondii in a cell-intrinsic manner. Further, genetic deletion of Stat1 from microglia during T. gondii challenge leads to fatal pathology despite largely equivalent or enhanced immune effector functions displayed by brain-infiltrating immune populations. Finally, we show that microglial STAT1-deficiency results in the overrepresentation of the highly replicative, lytic tachyzoite form of <em>T. gondii</em>, relative to its quiescent, semi-dormant bradyzoite form typical of chronic CNS infection. Our data suggest an overall protective role of CNS-resident microglia against<em> T. gondii</em> infection, illuminating (i) general mechanisms of CNS-specific immunity to infection (ii) and a clear role for IFN-STAT1 signaling in regulating a microglial activation phenotype observed across diverse neuroinflammatory disease states.</p>
Contrasting disease progression, microglia reactivity, tolerance, and resistance to Toxoplasma gondii infection in two mouse strains
<p><strong><span>Figure S1</span></strong><span>. Stereological Sampling: Low-power photomicrographs (A and B) displaying the molecular layer of the dentate gyrus, the area of interest, alongside the sampling grid (C). Additionally, a high-power photomicrograph (D) showcases IBA-1 immunolabeled microglia (the object of interest). Scale bar: A - 250µm, and D: 25µm.</span></p> <p> </p> <p><strong><span>Figure S2</span></strong><span>. The recovery of BALB/c microglia in the molecular layer of dentate gyrus was observed 43 days after infection. At this point, only minor morphological changes were observed, and all the morphological changes induced by <em>T. gondii</em> infection at 22 dpi have disappeared. The analysis methods used included hierarchical cluster analysis (A), discriminant function analysis (C and E), morphological complexity (B), and convex hull volume (D).</span></p>
Fig 5 in Docosahexaenoic Acid (DHA) Reduces LPS-Induced Inflammatory Response Via ATF3 Transcription Factor and Stimulates Src/Syk Signaling-Dependent Phagocytosis in Microglia
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Fig 3 in Docosahexaenoic Acid (DHA) Reduces LPSInduced Inflammatory Response Via ATF3 Transcription Factor and Stimulates Src/ Syk Signaling-Dependent Phagocytosis in Microglia
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Fig 4 in Docosahexaenoic Acid (DHA) Reduces LPS-Induced Inflammatory Response Via ATF3 Transcription Factor and Stimulates Src/Syk Signaling-Dependent Phagocytosis in Microglia
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Data for: Microglia phagocytosis determines the volume and function of the rat Sexually Dimorphic Nucleus of the Preoptic Area
<p>The Sexually Dimorphic Nucleus of the Preoptic Area (SDN-POA) is the oldest and most robust sex difference reported in mammalian brain and is singular for its presence across a wide range of species from rodents to ungulates to man. This small collection of Nissl dense neurons is reliably larger in volume in males. Yet, despite its notoriety and intense interrogation, both the mechanism establishing the sex difference and the functional role of the SDN have remained elusive. Convergent evidence from rodent studies led to the conclusion that testicular androgens aromatized to estrogens are neuroprotective in males and that higher apoptosis (naturally occurring cell death) in females determines their smaller SDN. In several species, including humans, a smaller SDN correlates with a preference for mating with males. We report here that this volume difference is dependent upon a participatory role of phagocytic microglia which engulf more neurons in the female SDN and assure their destruction . Selectively blocking microglia phagocytosis temporarily spared neurons from apoptotic death and increased SDN volume in females without hormone treatment. Increasing the number of neurons in the SDN in neonatal females resulted in loss of preference for male odors in adulthood, an effect paralleled by dampened excitation of SDN neurons as evidenced by reduced IEG expression when exposed to male urine. Thus, the mechanism establishing a sex difference in SDN volume includes an essential role for microglia, and SDN function as a regulator of sexual partner preference is confirmed.</p>
Human brain plaques and microglia dataset
<p>Data-set supporting our publication. The raw data was converted using the proposed pipeline and this data-set can be used to test the stitching, segmentation and analysis proposed in the paper.</p>
isoMiGA: Long-read isoforms discovered in human microglia
<p>https://github.com/RajLabMSSM/isoMiGA </p> <p>Novel isoform discovery from long-read RNA-seq of 30 human microglia samples with PacBio CCS.</p> <p><strong>Isoform sets used</strong></p> <p>isomiga_full: all isoforms discovered from hybrid assembly of long-read and short-read data</p> <p>isomiga_novel: just the novel isoforms</p> <p>isomiga_gencode: the novel isoforms combined with all isoforms in GENCODE v38.</p> <p>Not included: GENCODE v38 - available at https://www.gencodegenes.org/human/release_38.html</p> <p><strong>Isoform coordinates (GTF)</strong></p> <p>All files bgzipped and tabixed for easy random access by IGV. {file}.gtf.gz is the Isoform list, {file}.gtf.gz.tbi is the tabix index.</p> <p><strong>Isoform sequences (FASTA)</strong></p> <p>All files gzipped. </p> <p> </p>
Role of Microglia in the Pathogenesis of Progressive Multiple Sclerosis
ClinicalTrials.gov study NCT03134716. IPD Sharing: UNDECIDED. Countries: 1. Publications: 2.
Multicenter Study Using IMC to Analyze the Impact of ICANS on Microglia
ClinicalTrials.gov study NCT05811117. IPD Sharing: NO. Countries: 1. Publications: 1.
Sex differences in prefrontal cortex microglia morphology: impact of a two-hit model of adversity throughout development
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Human myelinated brain organoids with integrated microglia as a model for myelin repair and remyelinating therapies
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Immune responses in mice lacking STAT-1 in microglia
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Data for: Microglia phagocytosis determines the volume and function of the rat Sexually Dimorphic Nucleus of the Preoptic Area
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Microglia resting
Drawing uploaded to scidraw.io on: 21 May 2020
Microglia reactive
Drawing uploaded to scidraw.io on: 21 May 2020
Local externalization of phosphatidylserine mediates developmental synaptic pruning by microglia
<p>Neuronal circuit assembly requires the fine balance between synapse formation and elimination. Microglia, through the elimination of supernumerary synapses, have an established role in this process. While the microglial receptor TREM2 and the soluble complement proteins C1q and C3 are recognized as key players, the neuronal molecular components that specify synapses to be eliminated are still undefined. Here, we show that exposed phosphatidylserine (PS) represents a neuronal "eat-me" signal involved in microglial-mediated pruning. In hippocampal neuron and microglia co-cultures, synapse elimination can be partially prevented by blocking accessibility of exposed PS using Annexin V or through microglial loss of TREM2. In vivo, PS exposure at both hippocampal and retinogeniculate synapses and engulfment of PS-labeled material by microglia occurs during established developmental periods of microglial-mediated synapse elimination. Mice deficient in C1q, which fail to properly refine retinogeniculate connections, have elevated presynaptic PS exposure and reduced PS engulfment by microglia. These data provide mechanistic insight into microglial-mediated synapse pruning and identify a novel role of developmentally regulated neuronal PS exposure that is common among developing brain structures.</p>
ScienceDex guides
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These curated guides explain access requirements, typical timelines, costs, and reuse considerations for widely used research datasets.
Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
Annotated Behaviour and Observability Dataset (ABODe)
ABODe is a University of Edinburgh DataShare dataset for behavior classification in group-housed mice using home-cage video, identities, bounding boxes, ground-plate positions, and annotator labels.
DANDI Archive for NWB datasets
DANDI is a BRAIN Initiative archive for publishing and sharing neurophysiology data, including electrophysiology, optophysiology, and behavioral data packaged as NWB and related standards.
International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.