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362 results for “neuroinflammation”
Unveiling the role of miRNAs from MSC-EVs in neuroinflammation and behavioral impairments induced by chronic alcohol consumption
<p><strong>Part of the project: "Unveiling the role of miRNAs from MSC-EVs in neuroinflammation and behavioral impairments induced by chronic alcohol consumption."</strong></p> <p>This dataset contains small RNA sequencing data derived from extracellular vesicles (EVs) isolated from human adipose tissue-derived mesenchymal stem cells (MSC-EVs). The data was generated to study the potential therapeutic effects of repeated intravenous administration of MSC-EVs on neuroinflammation, cognitive dysfunction, and addictive-like behaviors induced by chronic alcohol consumption.</p> <p>Total RNA from MSC-EVs was extracted using the Total Exosome RNA Isolation Kit (Invitrogen). Small RNA libraries were constructed with the Small RNA-Seq Library Prep Kit (Lexogen) and sequenced on the Illumina NextSeq 550 platform with a 1 x 150 bp read length. The raw sequencing data are provided in fastq format.</p> <p> </p> <div> </div>
Raw data to "Blunting neuroinflammation with resolvin D1 prevents early pathology in a rat model of Parkinson's disease"
<p>Background: In vivo treatment of animals with anti-inflammatory and pro-resolving mediators (SPMs) could be counteracted by their limited in vivo bioavailability due to their unstable nature as lipids that can undergo oxidation or enzymatic degradation.</p> <p>Results: Thus, we performed a time course of RvD1 plasma levels over 36 hours after an initial intraperitonael injection of this lipid mediator at a concentration of 200 ng/animal. After a single injection the plasma concentration of RvD1 peaked at 1h (~360 pg/ml), stayed almost constant at 3h(~360 pg/ml), halved its levels after 6h (~180 pg/ml) and slowly returned close to the baseline after 36h (~30 pg/ml). These results indicate that RvD1 is rapidly distributed into the bloodstream and eliminated from the vascular compartment due to metabolism and/or diffusion into the blood–brain barrier.</p> <p>Conclusions: These findings are important to define route and timing of in vivo administration of SPMs in order to maintain sufficient levels to sustain biological activities both in the periphery and within the central nervous system.</p>
Deferoxamine Regulates Neuroinflammation and Iron Homeostasis in a Mouse Model of Postoperative Cognitive Dysfunction
<p>The raw data of the manuscript” Deferoxamine Regulates Neuroinflammation and Iron Homeostasis in a Mouse Model of Postoperative Cognitive Dysfunction”</p>
Whole-transcriptome sequencing identifies neuroinflammation, metabolism and blood-brain barrier related processes in the hippocampus of aged mice during perioperative period
<p><span><strong>Aim</strong>:</span><span> Perioperative neurocognitive disorders (PND) occur frequently after surgery and anesthesia, especially in aged patients. Previous studies have shown multiple PND related mechanisms in the hippocampus, however, their relationships remain unclear. Meanwhile, the perioperative neuropathological processes are sophisticated and changeable, single period study could not reveal the accurate mechanisms. Thus, multiperiod whole-transcriptome study is necessary to elucidate the gene expression patterns during perioperative period.</span></p> <p><span><strong>Methods</strong>: </span><span>Aged</span><span> C57BL/6 mice were subjected to exploratory laparotomy under sevoflurane anesthesia. Whole-transcriptome sequencing (RNA-seq analysis) was performed on the hippocampi from control condition (Con), 30 minutes (Day0), 2 days (Day2) and 7 days (Day7) after surgery. Gene Ontology</span><span>/Kyoto Encyclopedia of Genes and Genomes analyses,</span><span> quantitative Real-Time PCR, immunofluorescence and fear conditioning test were also performed to elucidate the pathological processes and modulation networks during the period.</span></p> <p><span><strong>Results</strong>: </span><span>Through RNA-seq analysis, 328, 3597 and 4179 differentially expressed genes (DEGs) were screened out in intraoperative period (Day0 vs Con), early postoperative period (Day2 vs Day0) and late postoperative period (Day7 vs Day2). The involved GO biological processes were divided into 9 categories, and positive-regulated processes were more than negative-regulated ones. Seventy-four transcription factors were highlighted. The potential synaptic and neuroinflammatory pathways were constructed for Neurotransmitter, Synapse and Neuronal alteration categories with 9 DEGs (<em>Htr1a, Rims1, Ezh2,</em> etc.). The metabolic and mitochondrial pathways were constructed for Metabolism, Oxidative stress and Biological rhythm categories with 9 DEGs (<em>Gpld1, Sirt1, Cry2, </em>etc.). The blood-brain barrier and neurotoxicity related pathways were constructed for Blood-brain barrier, Neurotoxicity and Cognitive function categories with 10 DEGs (<em>Mmp2, Itpr1, Nrf1, </em>etc.).</span></p> <p><span><strong>Conclusion</strong>:</span><span> The results revealed gene expression patterns and modulation networks in the aged hippocampus during perioperative period, which provide insights into overall mechanisms and potential therapeutic targets for prevention and treatment of perioperative central nervous system diseases, such as PND, from the genetic level.</span></p>
Data from: HIF prolyl hydroxylase 2/3 deletion disrupts astrocytic integrity and exacerbates neuroinflammation
<p><span>Astrocytes constitute the parenchymal border of the blood-brain barrier (BBB), modulate the exchange of soluble and cellular elements, and are essential for neuronal metabolic support. Thus, astrocytes critically influence neuronal network integrity. In hypoxia, astrocytes upregulate a transcriptional program that has been shown to boost neuroprotection in several models of neurological diseases. We investigated transgenic mice with astrocyte-specific activation of the hypoxia-response program by deleting the oxygen sensors, HIF prolyl-hydroxylase domains 2 and 3 (Phd2/3). We induced Phd2/3 deletion in experimental autoimmune encephalomyelitis (EAE) in a therapeutic approach that led to an exacerbation of the disease mediated by massive immune cell infiltration. We found that Phd2/3-ko astrocytes, though expressing a neuroprotective signature, exhibited a gradual loss of gap-junctional Connexin-43 (Cx43), which was induced by vascular endothelial growth factor-alpha (Vegf-a) expression. These results provide mechanistic insights into astrocyte biology, their critical role in hypoxic states, and in chronic inflammatory CNS diseases.</span></p>
Assessing Neuroinflammation in GWI Using MRS
ClinicalTrials.gov study NCT04638998. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Cannabidiol for Reduction of Brain Neuroinflammation
ClinicalTrials.gov study NCT05066308. IPD Sharing: YES. Countries: 1. Publications: 1.
Evaluating the Role of Neuroinflammation in Low Back Pain
ClinicalTrials.gov study NCT03106740. IPD Sharing: NO. Countries: 1. Publications: 4.
To Assess Neuroinflammation and Neurocognitive Function in Patients With Acute Hepatitis C and Chronic HIV Co-Infection
ClinicalTrials.gov study NCT00959166. IPD Sharing: NO. Countries: 1. Publications: 1.
Whole-transcriptome sequencing identifies neuroinflammation, metabolism and blood-brain barrier related processes in the hippocampus of aged mice during perioperative period
Open the record for dataset details and reuse information.
Data from: HIF prolyl hydroxylase 2/3 deletion disrupts astrocytic integrity and exacerbates neuroinflammation
Open the record for dataset details and reuse information.
Data from: Gut microbiota regulate motor deficits and neuroinflammation in a model of Parkinson's disease
The intestinal microbiota influence neurodevelopment, modulate behavior, and contribute to neurological disorders. However, a functional link between gut bacteria and neurodegenerative diseases remains unexplored. Synucleinopathies are characterized by aggregation of the protein α-synuclein (αSyn), often resulting in motor dysfunction as exemplified by Parkinson's disease (PD). Using mice that overexpress αSyn, we report herein that gut microbiota are required for motor deficits, microglia activation, and αSyn pathology. Antibiotic treatment ameliorates, while microbial re-colonization promotes, pathophysiology in adult animals, suggesting that postnatal signaling between the gut and the brain modulates disease. Indeed, oral administration of specific microbial metabolites to germ-free mice promotes neuroinflammation and motor symptoms. Remarkably, colonization of αSyn-overexpressing mice with microbiota from PD-affected patients enhances physical impairments compared to microbiota transplants from healthy human donors. These findings reveal that gut bacteria regulate movement disorders in mice and suggest that alterations in the human microbiome represent a risk factor for PD.
Single-cell RNA sequencing of CNS-infiltrating HSC-derived phagocytes of Ms4a3Ai14, BM chimeric mice (CD45.2 Csf2rb-/-: CD45.1 Csf2rb+/+ and CD45.2 Ifngr1-/-: CD45.1 Ifngr1+/+) using 10X Genomics platform. IFN-γ and GM-CSF control complementary differentiation programs in the monocyte to phagocyte transition during neuroinflammation.
<p><strong>Single-cell RNA sequencing of CNS-infiltrating HSC-derived phagocytes of <em>Ms4a3</em><sup>Ai14</sup> at onset and peak EAE, BM chimeric mice (CD45.2 <em>Csf2rb</em><sup>-/-</sup>: CD45.1 <em>Csf2rb</em><sup>+/+</sup> and CD45.2 <em>Ifngr1<sup>-/-</sup></em>: CD45.1 <em>Ifngr1<sup>+/+</sup></em>) using 10X Genomics platform.</strong></p> <p>The sorted cells were loaded into 10x Genomics Chromium in parallel. Libraries were prepared as per the manufacturer's protocol (Chromium Next GEM Single Cell 3ʹ Reagent Kits v3.1 protocol) and sequenced on an Illumina NovaSeq sequencer according to 10X Genomics recommendations (paired-end reads, R1=28, i7=8, R2=91) to a depth of around 50,000 reads per cell.</p> <p>Initial processing was done using Cell Ranger (v3.1.0) mkfastq and count (reads were aligned to GENCODE reference build GRCm38.p6 Release M23 with added tdTomato sequence for the dataset from <em>Ms4a3</em><sup>Ai14</sup> mouse and collapse UMIs). Starting from the filtered gene-cell count matrix produced by CellRranger's in-built cell calling algorithms, we proceeded with Seurat v4 workflow.</p>
Single-cell RNA sequencing of Lymph node-infiltrating HSC-derived phagocytes of Ms4a3Ai14 using 10X Genomics platform. IFN-γ and GM-CSF control complementary differentiation programs in the monocyte to phagocyte transition during neuroinflammation.
<p><strong>Single-cell RNA sequencing of Lymph node-infiltrating HSC-derived phagocytes of <em>Ms4a3</em><sup>Ai14</sup> at onset and peak EAE using 10X Genomics platform.</strong></p> <p>The sorted cells were loaded into 10x Genomics Chromium in parallel. Libraries were prepared as per the manufacturer's protocol (Chromium Next GEM Single Cell 3ʹ Reagent Kits v3.1 protocol) and sequenced on an Illumina NovaSeq sequencer according to 10X Genomics recommendations (paired-end reads, R1=28, i7=8, R2=91) to a depth of around 50,000 reads per cell.</p> <p>Initial processing was done using Cell Ranger (v3.1.0) mkfastq and count (reads were aligned to GENCODE reference build GRCm38.p6 Release M23 with added tdTomato sequence for the dataset from <em>Ms4a3</em><sup>Ai14</sup> mouse and collapse UMIs). Starting from the filtered gene-cell count matrix produced by CellRranger's in-built cell calling algorithms, we proceeded with Seurat v4 workflow.</p>
Single-cell RNA sequencing of Bone Marrow-infiltrating HSC-derived phagocytes of Ms4a3Ai14 using 10X Genomics platform. IFN-γ and GM-CSF control complementary differentiation programs in the monocyte to phagocyte transition during neuroinflammation.
<p><strong>Single-cell RNA sequencing of Bone Marrow-infiltrating HSC-derived phagocytes of <em>Ms4a3</em><sup>Ai14</sup> at onset and peak EAE using 10X Genomics platform.</strong></p> <p>The sorted cells were loaded into 10x Genomics Chromium in parallel. Libraries were prepared as per the manufacturer's protocol (Chromium Next GEM Single Cell 3ʹ Reagent Kits v3.1 protocol) and sequenced on an Illumina NovaSeq sequencer according to 10X Genomics recommendations (paired-end reads, R1=28, i7=8, R2=91) to a depth of around 50,000 reads per cell.</p> <p>Initial processing was done using Cell Ranger (v3.1.0) mkfastq and count (reads were aligned to GENCODE reference build GRCm38.p6 Release M23 with added tdTomato sequence for the dataset from <em>Ms4a3</em><sup>Ai14</sup> mouse and collapse UMIs). Starting from the filtered gene-cell count matrix produced by CellRranger's in-built cell calling algorithms, we proceeded with Seurat v4 workflow.</p>
Single-cell RNA sequencing of Blood-infiltrating HSC-derived phagocytes of Ms4a3Ai14 using 10X Genomics platform. IFN-γ and GM-CSF control complementary differentiation programs in the monocyte to phagocyte transition during neuroinflammation.
<p><strong>Single-cell RNA sequencing of Blood-infiltrating HSC-derived phagocytes of <em>Ms4a3</em><sup>Ai14</sup> at onset and peak EAE using 10X Genomics platform.</strong></p> <p>The sorted cells were loaded into 10x Genomics Chromium in parallel. Libraries were prepared as per the manufacturer's protocol (Chromium Next GEM Single Cell 3ʹ Reagent Kits v3.1 protocol) and sequenced on an Illumina NovaSeq sequencer according to 10X Genomics recommendations (paired-end reads, R1=28, i7=8, R2=91) to a depth of around 50,000 reads per cell.</p> <p>Initial processing was done using Cell Ranger (v3.1.0) mkfastq and count (reads were aligned to GENCODE reference build GRCm38.p6 Release M23 with added tdTomato sequence for the dataset from <em>Ms4a3</em><sup>Ai14</sup> mouse and collapse UMIs). Starting from the filtered gene-cell count matrix produced by CellRranger's in-built cell calling algorithms, we proceeded with Seurat v4 workflow.</p>
Supplementary File of "Effect of Renal Ischemia Reperfusion on Brain Neuroinflammation"
<p>Supplementary File of "Effect of Renal Ischemia Reperfusion on Brain Neuroinflammation"</p>
MRI Dataset: Diffusion MRI as a potential non-invasive biomarker of neuroinflammation following intracerebral haemorrhage
<p>Raw MRI dataset of T2 and NODDI scans.</p> <p>Subjects: Adult male Sprague-Dawley rats, aged 10-12 weeks, 300-450g. Subjected to intracerebral haemorrhage induction by intracranial injection of 0.2 Type VII collagenase, recovered for 7 days prior to these MRI scans being performed. Further methodological information available upon request.</p>
MRS to Determine Neuroinflammation and Oxidative Stress in MPS I
ClinicalTrials.gov study NCT03576729. IPD Sharing: YES. Countries: 1. Publications: 2.
Neuroinflammation in Hypertension Study
ClinicalTrials.gov study NCT04478500. IPD Sharing: NO. Countries: 1. Publications: 2.
ScienceDex guides
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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.