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2,706 results for “Mouse model”
Adenosine deficiency facilitates CA1 synaptic hyperexcitability in the presymptomatic phase of a mouse KI model of Alzheimer disease.
<p><span>All data points, statistical models and raw western blot images from "Adenosine deficiency facilitates CA1 synaptic hyperexcitability in the presymptomatic phase of a mouse KI model of Alzheimer disease" are available. </span></p>
Multiomics Analysis of the mdx/mTR Mouse Model of Duchenne Muscular Dystrophy
<p>This dataset contains RNA sequencing, proteomics, metabolomics, lipidomics, primer sequence, and Ingenuity Pathway Analysis data for a study evaluating differences between the transcriptome, proteome, metabolome, and lipidome of lower limb muscles of mdx/mTR (Jackson Labs strain 023535) and wild-type C57BL/6J (Jackson Labs strain 000664) mice. Updated from previous submission, DOI: 10.5281/zenodo.3370799.</p>
Spatiotemporal dysregulation of neuron-glia related genes and pro-/anti-inflammatory miRNAs in the 5xFAD mouse model of Alzheimer's disease - Supplementary data
<p><strong>Supplementary Table 1. </strong> Gene expression profile by RT-qPCR analysis revealed no significant differences when simultaneously considering the genotype (WT/5xFAD), age (6/9 months) and brain region (HPC, hippocampus/PFC, prefrontal cortex). </p> <p><strong>Supplementary Table 2.</strong> miRNA-target table for the Analyzed microRNAs and targets selected for this study. Obtained in the online platform https://www.mirnet.ca/</p> <p><strong>Supplementary Table 3. </strong> Node table for the analyzed microRNAs and targets selected for this study. We only considered miRNAs and/or targets with a node degree of at least 2. Obtained in the online platform https://www.mirnet.ca/</p> <p><strong>Supplementary Table 4.</strong> Bivariate Pearson’s correlation coefficients and respective p-values obtained between all miRNAs and genes.</p> <p><strong>Supplementary Table 5.</strong> List of microRNAs analyzed by RT-qPCR and their primer sequences.</p> <p><strong>Supplementary Table 6.</strong> List of genes and respective primer sequences used for mRNA analysis by RT-qPCR.</p> <p><strong>Supplementary Table 7.</strong> Raw data used for correlational analysis in hippocampus (HPC) and prefrontal cortex (PFC) using the cor function in RStudio software.</p>
10X Single Cell RNA-Seq On WT and Mutation mouse models
<p>Four four-week-old mice, consisting of wild type, Pten mutation, MAP3K3 mutation, and MAP3K3+Pten mutation, were sampled at 4 weeks of age. Endothelial cells were enriched using CD31 magnetic beads, followed by 10X single-cell RNA sequencing.</p>
Dataset related to article "Fluoxetine rescues rotarod motor deficits in Mecp2 heterozygous mouse model of Rett syndrome via brain serotonin"
<p><em>The file contains raw data related to the article "Fluoxetine rescues rotarod motor deficits in Mecp2 heterozygous mouse model of Rett syndrome via brain serotonin", available from </em><a href="https://doi.org/10.1016/j.neuropharm.2020.108221">https://doi.org/10.1016/j.neuropharm.2020.108221</a><em>.</em></p> <p> </p> <p><strong>Abstract of the manuscript</strong></p> <p> Motor skill is a specific area of disability of Rett syndrome (RTT), a rare disorder occurring almost exclusively in girls, caused by loss-of-function mutations of the X-linked methyl-CpG-binding protein2 (MECP2) gene, encoding the MECP2 protein, a member of the methyl-CpG-binding domain nuclear proteins family. Brain 5-HT, which is defective in RTT patients and Mecp2 mutant mice, regulates motor circuits and SSRIs enhance motor skill learning and plasticity. In the present study, we used heterozygous (Het) Mecp2 female and Mecp2-null male mice to investigate whether fluoxetine, a SSRI with pleiotropic effects on neuronal circuits, rescues motor coordination deficits. Repeated administration of 10 mg/kg fluoxetine fully rescued rotarod deficit in Mecp2 Het mice regardless of age, route of administration or pre-training to rotarod. The motor improvement was confirmed in the beam walking test while no effect was observed in the hanging-wire test, suggesting a preferential action of fluoxetine on motor coordination. Citalopram mimicked the effects of fluoxetine, while the inhibition of 5-HT synthesis abolished the fluoxetine-induced improvement of motor coordination. Mecp2 null mice, which responded poorly to fluoxetine in the rotarod, showed reduced 5-HT synthesis in the prefrontal cortex, hippocampus and striatum, and reduced efficacy of fluoxetine in raising extracellular 5-HT as compared to female mutants. No sex differences were observed in the ability of fluoxetine to desensitize 5-HT<sub>1A</sub> autoreceptors upon repeated administration. These findings indicate that fluoxetine rescues motor coordination in Mecp2 Het mice through its ability to enhance brain 5-HT and suggest that drugs enhancing 5-HT neurotransmission may have beneficial effects on motor symptoms of RTT.</p>
The secretome atlas of two mouse models of progeria
<p>Hutchinson-Gilford progeria syndrome (HGPS) is a rare genetic disease caused by nuclear envelope alterations that lead to accelerated aging and premature death. Several studies have linked health and longevity to cell-extrinsic mechanisms, highlighting the relevance of circulating factors in the aging process as well as in age related diseases. We performed a global plasma proteomic analysis in two preclinical progeroid models (<em>Lmna<sup>G609G/G609G</sup></em> and <em>Zmpste24<sup>-/-</sup></em> mice) using aptamer-based proteomic technology. Pathways related to the extracellular matrix, growth factor response and calcium ion binding were among the most enriched in the proteomic signature of progeroid samples compared to controls. Despite the global down-regulation trend found in the plasma proteome of progeroid mice, several proteins associated with cardiovascular disease, the main cause of death in HGPS, were up-regulated. We also developed a chronological age predictor using plasma proteome data from a cohort of healthy mice (aged 1-30 months), that reported an age acceleration when applied to progeroid mice, indicating that these mice exhibit an ‘old’ plasma proteomic signature. Furthermore, when compared to naturally-aged mice, a great proportion of differentially expressed circulating proteins in progeroid mice were specific to premature aging, highlighting secretome-associated differences between physiological and accelerated aging. This is the first large-scale profiling of the plasma proteome in progeroid mice, which provides an extensive list of candidate circulating plasma proteins as potential biomarkers and/or therapeutic targets for further exploration and hypothesis generation in the context of both physiological and premature aging.</p>
Predicting the distribution of serotonergic axons: A supercomputing simulation of reflected fractional Brownian motion in a 3D-mouse brain model
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A selective small-molecule agonist of G protein-gated inwardly-rectifying potassium channels reduces epileptiform activity in a mouse model of tumor associated epilepsy - Thy1-GCaMP Tumor Electrophysiology
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Perirhinal cortex abnormalities impair hippocampal plasticity and learning in Scn2a, Fmr1, and Cdkl5 autism mouse models
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Retinal proteome profiling of inherited retinal degeneration across three different mouse models suggests common drug targets in retinitis pigmentosa
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Computational IHC-H&E mapping in mouse models of colitis (IHC WSIs from paired H&E-IHC WSIs, Part 1/2)
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Slow and fast cortical cholinergic arousal is reduced in a mouse model of focal seizures with impaired consciousness
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Computational IHC-H&E mapping in mouse models of colitis (H&E WSIs from paired H&E-IHC WSIs)
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Data from: Longitudinal three-photon imaging for tracking amyloid plaques and vascular degeneration in a mouse model of Alzheimer’s disease
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Computational IHC-H&E mapping in mouse models of colitis (IHC WSIs from paired H&E-IHC WSIs, Part 2/2)
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Gene drives for vertebrate pest control: realistic spatial modelling of eradication probabilities and times for island mouse populations
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Gut bacteria from multiple sclerosis patients modulate human T cells and exacerbate symptoms in mouse models
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Longitudinal analysis of the microbiome and metabolome in the 5xfAD mouse model of Alzheimer's disease
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Novel DMD mouse model carrying a multi-exonic Dmd deletion exhibit progressive muscular dystrophy and early-onset cardiomyopathy
Duchenne muscular dystrophy (DMD) is a life-threatening neuromuscular disease caused by the lack of dystrophin, resulting in progressive muscle wasting and locomotor dysfunctions. By adulthood, almost all patients also develop cardiomyopathy, which is the primary cause of death in DMD. While there has been extensive effort in creating animal models to study treatment strategies for DMD, most fail to recapitulate the complete skeletal and cardiac disease manifestations that are presented in affected patients. Here, we generated a mouse model mirroring a patient deletion mutation of exons 52-54 (<i>Dmd &[Delta]52-54</i>). The <i>Dmd &[Delta]52-54</i> mutation led to the absence of dystrophin, resulting in progressive muscle deterioration with weakened muscle strength. Moreover, <i>Dmd &[Delta]52-54</i> present with early-onset cardiomyopathy which is absent in current pre-clinical dystrophin deficient mouse models. Therefore, <i>Dmd &[Delta]52-54</i> presents itself as an excellent pre-clinical model to evaluate the impact on skeletal and cardiac muscles for both mutation dependent and independent approaches.
Ectopic expression of BBS1 rescues male infertility, but not retinal degeneration, in a BBS1 mouse model
<p>Bardet-Biedl syndrome (BBS) is a rare ciliopathy for which there are no current effective treatments. BBS is a genetically heterogeneous disease, though the M390R mutation in <i>BBS1 </i>is involved in approximately 25% of all genetic diagnoses of BBS. The principle features of BBS include retinal degeneration, obesity, male infertility, polydactyly, intellectual disability, and renal abnormalities. Patients with mutations in BBS genes often present with night blindness within the first decade of life, which progresses to complete blindness. This is due to progressive loss of photoreceptor cells. Male infertility is caused by a lack of spermatozoa flagella, rendering them immobile. In this study, we have crossed the wild-type human <i>BBS1</i> gene, driven by the CAG promoter, onto the <i>Bbs1<sup>M390R/M390R </sup></i>mouse model to determine if ectopic expression of <i>BBS1</i> rescues male infertility and retinal degeneration. qRT-PCR indicates that the <i>BBS1 </i>transgene is expressed in multiple tissues throughout the mouse, with the highest expression seen in the testes, and much lower expression in the eye and hypothalamus. Immunohistochemistry of the transgene in the eye showed little if any expression in the photoreceptor outer nuclear layer. When male <i>Bbs1<sup>M30R/M390R</sup>;BBS1<sup>TG+</sup></i>mice are housed with WT females, they are able to sire offspring, indicating that the male infertility phenotype of BBS is rescued by the transgene. Using electroretinography (ERGs) to measure retinal function and optical coherence tomography to measure retinal thickness, we show that the transgene does not confer protection against retinal degeneration in <i>Bbs1<sup>M300R/M390R</sup>;BBS1<sup>TG+ </sup></i>mice.</p>
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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.