Find research datasets worth reusing
Search datasets from major research repositories and use ShareScore to quickly assess how well each record supports discovery, access, and reuse.
1,274
datasets available to search
ShareScore release 0.9.0
Dataset results
1,274 results for “disease models”
DATA to support Dyrk1a function in glutamatergic neurons in mouse models of Mental Retardation Disease 7 (MRD7) and Down syndrome (or trisomy 21)
<p>Four datasets are provided here to support the function of Dyrk1a in glutamatergic neurons in mouse models of Mental Retardation Disease 7 (MRD7) and Down syndrome (or trisomy 21):</p> <p>- RNAseq data to compare hippocampal expressed genes at postnatal day 30, in the complete inactivation of Dyrk1a in glutamatergic neurons using a Dyrk1a floxed-allele and the Camk2:Cre transgene</p> <p>- data from all the figures</p> <p>-data from all the supplementary figures </p> <p>-data from the quantitative proteomic analysis made from hippocampal extract of wt, Dyrk1a heterozygote, Dp(16)1Yey and Dp(16)1Yey with only two functional copies of Dyrk1a</p> <p>Detailed information are available in the article by Brault et al 2021, deposited in Biorachiv https://doi.org/10.1101/2021.05.01.442242 </p>
Allele-specific quantitation of ATXN3 and HTT transcripts in polyQ disease models.
<p>Precise values obtained during the research that led to the publishing of scientific paper entitled 'Allele-specific quantitation of ATXN3 and HTT transcripts in polyQ disease models'.</p>
Data from: Chronic Rapamycin administration via drinking water mitigates the pathological phenotype in a Krabbe disease mouse model through autophagy activation.
<p>ABSTRACT </p><p>Krabbe disease (KD) is a rare disorder caused by a deficiency of the lysosomal enzyme galactosylceramidase (GALC), resulting in the accumulation of the cytotoxic metabolite psychosine (PSY) in the nervous system. This accumulation triggers demyelination and neurodegeneration. Despite ongoing research, the underlying pathogenic mechanisms remain incompletely understood, and there is currently no cure available.</p><p>Previous studies from our lab revealed the presence of autophagy dysfunctions in KD pathogenesis, as evidenced by the presence of p62-tagged protein aggregates in the brains of KD mice and increased p62 levels in the KD sciatic nerve. We also demonstrated that the autophagy inducer Rapamycin (RAPA) can partially restore the wild-type (WT) phenotype in KD primary cells by reducing the number of p62 aggregates.</p><p>In this study, we tested RAPA in the Twitcher (TWI) mouse, a spontaneous KD mouse model. We administered the drug ad libitum via drinking water (15 mg/L) starting from post-natal day (PND) 21-23. We longitudinally monitored the motor performance of the mice through grip strength and rotarod tests, along with various biochemical parameters related to KD pathogenesis (i.e. autophagy markers expression, myelination, astrogliosis, and PSY accumulation).</p><p>Our findings demonstrate that RAPA significantly enhances motor functions at specific treatment time points and reduces astrogliosis in TWI brain, spinal cord, and sciatic nerves. Using western blot and immunohistochemistry, we observed a decrease in p62 aggregates in TWI nervous tissues, which corroborates our earlier in-vitro results. Furthermore, RAPA treatment partially reduces PSY levels in the spinal cord.</p><p>In conclusion, our results support the consideration of RAPA as a supportive therapy for KD. Importantly, as RAPA is already available in pharmaceutical formulations for clinical use, its potential for KD treatment can be promptly evaluated in clinical trials.</p>
Interviews for New Business Models for Pharmaceutical Innovation and Access to Medicines - Rare Diseases
<p>These supplementary materials represent the partial dataset in the form of semi-structured interviews, collected and analyzed in the research article "Alternative innovation models of pharmaceutical development for rare disease drugs: how (and) do they work?: A qualitative study". This article is one of the outcomes of the "New Business Models for Pharmaceutical Innovation and Global Access to Medicines" research project, conducted at the Global Health Center, within the Geneva Graduate Institute. The dataset contains 10/11 interviews collected and used in this article, which are published with the informed consent of the interviewees.</p> <p>Details about the research project can be found at: <a href="https://www.graduateinstitute.ch/NBM">https://www.graduateinstitute.ch/NBM</a></p>
Peripheral MC1R activation modulates immune responses and confers neuroprotection in a mouse model of Parkinson's disease
<p>Raw data sets for the manuscripts</p> <p>This work was supported by NIH grants R01NS102735 and R01NS110879, the Farmer Family Foundation Initiative for Parkinson’s Disease Research and the MJFF and ASAP [ASAP-000312].</p>
Integrative in situ mapping of single-cell transcriptional states and tissue histopathology in an Alzheimer disease model
<p>Amyloid-β plaques and neurofibrillary tau tangles are the neuropathologic hallmarks of Alzheimer’s disease (AD), but the spatiotemporal cellular responses and molecular mechanisms underlying AD pathophysiology remain poorly understood. Here we introduce STARmap PLUS to simultaneously map single-cell transcriptional states and disease marker proteins in brain tissues of AD mouse models at a voxel size of 95 95 350 nm. This high-resolution spatial transcriptomics map revealed a core-shell structure where disease-associated microglia (DAM) closely contact amyloid-β plaques, whereas disease-associated astrocyte-like cells (DAA-like) and oligodendrocyte precursor cells (OPC) are enriched in the outer shells surrounding the plaque-DAM complex. Hyperphosphorylated tau emerged mainly in excitatory neurons in the CA1 region accompanied by infiltration of oligodendrocyte subtypes into the axon bundles of hippocampal alveus. The integrative STARmap PLUS method bridges single-cell gene expression profiles with tissue histopathology at subcellular resolution, providing an unprecedented roadmap to pinpoint the molecular and cellular mechanisms of AD pathology and neurodegeneration.</p>
Biochemical Characterization of Mouse Retina of an Alzheimer's Disease Model by Raman Spectroscopy
<p>Raman raw data for the paper "Biochemical Characterization of Mouse Retina of an Alzheimer’s Disease Model by Raman Spectroscopy"</p> <ul> <li>two datasets of Raman images from cross-sectional and en face mouse retinas without processing</li> </ul>
Raw dataset and additional data for article "Nonmotor symptoms associated with progressive loss of dopaminergic neurons in a mouse model of Parkinson's disease"
<p>Dataset from the project investigating the presence of nonmotor symptoms of Parkinson's disease in a mouse model of progressive loss of dopaminergic neurons (namely,TIF-IADATCreERT2 strain). Mice were tested for executive and cognitive functions (males: Operant Sensation Seeking test, OSS; females: Probabilistic Reversal Learning Task in Intellicages), olfactory acuity (males: buried food test), saccharin preference (males and females), and motor performance (males and females: test using CatWalk apparatus).</p><p>The dataset includes files used to perform statistical analyses but their names may vary from the ones used in the scripts. For the purpose of recreating our analyses, please refer to the GitHub page, where both scripts and input data file names (in 'Raw data files' section) are compliant: https://github.com/annaradli/tif-pd-behavior.</p><p><strong>Description of files:</strong></p><p><i>Raw data files:</i></p><ul><li>animals_info.csv - animals data: genotype, sex, age, Intellicage tag identifier</li><li>catwalk_run_statistics_all_females.csv - data recorded in CatWalk apparatus for females</li><li>catwalk_run_statistics_all_males.csv - data recorded in CatWalk apparatus for males</li><li>females_weight_raw_data_revised.csv - females' body weight (revised for containing Polish words)</li><li>intellicage_raw_data.csv - data recorded in IntelliCage exported to .csv format</li><li>intellicage_raw_data_R.RData - data recorded in IntelliCage in .RData format</li><li>males_weight_raw_data.csv - males' body weight</li><li>olfactory_time_digging_raw_data.csv - time to start digging at the right place in the buried food test</li><li>olfactory_time_retrieve_raw_data.csv- time to retrieve cracker in the buried food test</li><li>oss_raw_data.csv - data recorded in the OSS test</li><li>saccharin_preference_males_raw_data.csv - saccharin preference test results for males</li><li>snvta_cells_count.csv - number of TH+ cells in SN and VTA in male mice (3+3) 14 weeks after tamoxifen treatment</li></ul><p><i>Additional data files:</i></p><ul><li>all_anova.xlsx - summary of two-way ANOVAs of all behavioral tests and weight measurements for males and females</li><li>catwalk_complete.xlsx - CatWalk complete dataset with datapoints</li><li>catwalk_correlation_between_paws.xlsx - correlation coefficients of CatWalk parameters between the left and right paws</li><li>catwalk_reduced.xlsx - CatWalk parameters used in linear regression model reduction of data</li><li>intelli.xlsx - IntelliCage data summarized in bins</li><li>oss.xlsx - operant sensation-seeking data</li></ul><p>v2 contains the corrected 'animals_info.csv' file without an unnecessary column.</p><p>v3 has a revised version of file containing females' weight measurements and also added a file with midbrain cell counts</p><p>v4 has a whole section of 'Additional data files' added</p>
Improving distribution models of sparsely-documented disease vectors by incorporating information on related species via joint modeling
<p>A necessary component of understanding vector-borne disease risk is the accurate characterization of the distributions of their vectors. Species distribution models have been successfully applied to data-rich species but may produce inaccurate results for sparsely-documented vectors. In light of global change, vectors that are currently not well-documented could become increasingly important, requiring tools to predict their distributions. One way to achieve this could be to leverage data on related species to inform the distribution of a<strong> </strong>sparsely-documented vector based on the assumption that the environmental niches of related species are not independent. Relatedly, there is a natural dependence of the spatial distribution of a disease on the spatial dependence of its vector. Here, we propose to exploit these correlations by fitting a hierarchical model jointly to data on multiple vector species and their associated human diseases to improve distribution models of sparsely-documented species. To demonstrate this approach, we evaluated the ability of twelve models—which differed in their pooling of data from multiple vector species and inclusion of disease data—to improve distribution estimates of sparsely-documented vectors. We assessed our models on two simulated data sets, which allowed us to generalize our results and examine their mechanisms. We found that when the focal species is sparsely documented, incorporating data on related vector species reduces uncertainty and improves accuracy by reducing overfitting. When data on vector species are already incorporated, disease data only marginally improve model performance. However, when data on other vectors are not available, disease data can improve model accuracy and reduce overfitting and uncertainty. We then assessed the approach on empirical data on ticks and tick-borne diseases in Florida and found that incorporating data on other vector species improved model performance. This study illustrates the value of exploiting correlated data via joint modeling to improve distribution models of data-limited species.</p>
Novel disease state model finds most juvenile green turtles develop and recover from fibropapillomatosis
<p>Fibropapillomatosis (FP) is a sea turtle disease characterized by benign tumor development on skin, eyes, and/or internal organs. It primarily affects juvenile green turtles (Chelonia mydas) in coastal foraging sites. The Indian River Lagoon (IRL), Florida, USA, is a coastal green turtle foraging site where the observed FP annual rate averaged 49% between 1983 and 2018. FP is not a major cause of sea turtle mortality and most individuals fully recover; however, the overall dynamics of this disease are poorly understood because prior disease history is unknown for individuals without FP at capture time, and future disease outcome is unknown for individuals with FP at capture time. To better evaluate FP dynamics for green turtles in the IRL, we developed a hierarchical model for predicting disease state change. We used data from 4,149 captures of 3,700 individual green turtles captured in the IRL. The hierarchical disease state model contained two levels: level one modeled whether an individual would develop FP, and level two modeled disease state progression, including states for pre-FP affliction, active FP affliction, and full recovery from FP. From the hierarchical model, we estimated 99.8% (95% credibility intervals 99.1-100%) of juvenile green turtles in the IRL developed FP, indicating that nearly every individual in the IRL is affected by this disease. The model also suggested that turtles quickly developed FP upon recruitment to the IRL and then recovered at different rates, with most completely recovering before emigrating from the IRL as they mature. This is the first analysis of long-term sea turtle data suggesting nearly every turtle in an aggregation both develops and recovers from FP.</p>
Development of a machine learning model to predict non- durable response to anti-TNF therapy in Crohn's disease using transcriptome imputed from genotypes
<p>This is the expression value predicted using PrediXcan version 7 to find a gene feature that can distinguish between patients with and without effect on infliximab.</p> <p>Among the various tissue models provided by PrediXcan v7, three models were selected and used: whole blood, Colon transverse, and terminal ileum of small intestine, and the predicted gene counts of each model were 6,294, 5,612 and 3,107.</p> <p>For each of the three models, predicted gene expression values and phenotype information per sample were submitted.</p>
Know what you don't know: Embracing state uncertainty in disease-structured multistate models
<p>Hidden Markov models (HMMs) are broadly applicable hierarchical models that derive their utility from separating state processes from observation processes yielding the data. Multistate models such as mark-recapture and dynamic multistate occupancy models are examples of HMMs that are frequently used in ecology. In their early formulations, states, such as pathogen infection status, were assumed to be perfectly observed without ambiguity in state assignment. However, state uncertainty is a pervasive feature of many ecological systems, and multievent models were developed to explicitly account for it.</p> <p>We developed a novel extended multievent mark-recapture model that incorporates state uncertainty at multiple levels of detection. Using a disease-structured example, both false-negative and false-positive state assignment errors are modeled at two levels of state assignment---the pathogen sampling process and the diagnostic process that samples are subjected to. We additionally describe methods to jointly model infection intensity to integrate heterogeneity in ecological parameters, such as survival, and the pathogen detection processes. We provide code to simulate and analyze datasets with various underlying ecological processes and fit our model to a mark-recapture dataset of <em>Mixophyes fleayi</em> (Fleay's barred frog) infected with the amphibian chytrid fungus (<em>Batrachochytrium dendrobatidis</em>, <em>Bd</em>).</p> <p>In our case study, we found evidence for various state assignment errors: the sampling protocol performed poorly in detecting <em>Bd</em>, pathogen detection was highly dependent on infection intensity, and false-positives were non-negligible. Incorporating state uncertainty yielded significantly higher estimates of infection prevalence and 4--5 times lower rates of infection state transitions compared to those obtained from a traditional multistate model.</p> <p>Our results highlight that incorporating state assignment errors improves inference on the ecological state process, especially when sensitivity and specificity of the state assignment processes are low. The general model structure can be applied to other HMMs, providing a foundation for modeling state uncertainty in a range of related models. --</p>
High-Resolution Vector-borne Disease Infection Risk Mapping with Area-to-Point Kriging and Species Distribution Modeling - Datasets
<p>Datasets and notebooks used in the publication High-Resolution Vector-borne Disease Infection Risk Mapping with Area-to-Point Kriging and Species Distribution Modeling</p>
Impact of infectious diseases on wild bovidae populations in Thailand: Insights from population modelling and disease dynamics
<p>The wildlife and livestock interface is vital for wildlife conservation and habitat management. Infectious diseases maintained by domestic species may impact threatened species such as Asian bovids, as they share natural resources and habitats. To predict the population impact of infectious diseases with different traits, we used stochastic mathematical models to simulate the population dynamics over 100 years for 100 times a model gaur (<em>Bos gaurus</em>) population with and without disease. We simulated repeated introductions from a reservoir, such as domestic cattle. We selected six bovine infectious diseases; anthrax, bovine tuberculosis, hemorrhagic septicaemia, lumpy skin disease, foot and mouth disease and brucellosis, all of which have caused outbreaks in wildlife populations. From a starting population of 300, the disease-free population increased by an average of 228% over 100 years. Brucellosis with frequency-dependent transmission showed the highest average population declines (-97%), with population extinction occurring 16% of the time. Foot and mouth disease with frequency-dependent transmission showed the lowest impact, with an average population increase of 200%. Overall, acute infections with very high or low fatality had the lowest impact, whereas chronic infections produced the greatest population decline. These results may help disease management and surveillance strategies support wildlife conservation.</p>
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>
BRAIN Journal-Prediction of Thyroid Disease Using Data Mining Techniques-Figure 2. Attributes of the classification models used in the experiments
<p>The authors used for their experiments a data set (UCI, 2016) containing 756 records about persons with thyroid dysfunctions. The classification model has 22 attributes; the class attribute is the target and it has three possible values: hypothyroidism, hyperthyroidism and normal. The current data set was extracted and preprocessed from the original file. A description of the attributes used in the experiments is given in Figure 2 (an extract from thyroid.arff test file). </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>
Analyses of metabolite profiling of Drosophila Parkinson's Disease model for identifying novel glial-based therapeutic targets
<p>Analysis for genetic screening and metabolomics identify glial adenosine metabolism as a therapeutic target in Parkinson’s disease</p> <p>This project contains the analysis of metabolite abundance measurements obtained with four different liquid chromatography mass spectrometry methods of synuclein expressing or control or fly brains in a wilde type or Adk1 knockout background.</p> <p> </p> <div> <h2>Table of contents</h2> <a href="https://github.com/jravilap/Olsen_Analyses#table-of-contents"></a></div> <div> <h3>Prerequisites</h3> <a href="https://github.com/jravilap/Olsen_Analyses#prerequisites"></a></div> <ul> <li>R (version 4.3.1 or higher)</li> <li>RStudio (optional, but recommended)</li> </ul> <div> <h3>R Packages</h3> <a href="https://github.com/jravilap/Olsen_Analyses#r-packages"></a></div> <p>The following R packages are required. You can install them using the commands below:</p> <div> <pre>install.packages(c(<span><span>"</span>readxl<span>"</span></span>, <span><span>"</span>calibrate<span>"</span></span>, <span><span>"</span>dplyr<span>"</span></span>, <span><span>"</span>ggplot2<span>"</span></span>))</pre> <div> </div> </div> <div> <h3>Package versions</h3> <a href="https://github.com/jravilap/Olsen_Analyses#package-versions"></a></div> <ul> <li>ggplot2_3.5.1</li> <li>dplyr_1.1.4</li> <li>yaml_2.3.8</li> <li>calibrate_1.7.7</li> <li>readxl_1.4.3</li> </ul> <div> <h2>Project Structure</h2> <a href="https://github.com/jravilap/Olsen_Analyses#project-structure"></a></div> <ul> <li><code>code/</code>: Contains the R scripts for the analysis.</li> <li><code>data/</code>: Processed data files. <ul> <li><code>22_0322_alphaSyn_fly_pilot_Classes.xlsx</code>: metabolite profiling data</li> <li><code>dup_metabs_decision.csv</code>: Table defining which metabolites profiled in more than one method should be used.</li> </ul> </li> <li><code>results/</code>: Output files, including plots and tables.</li> <li><code>common_functions/</code>: Custom R functions used in the analysis.</li> <li><code>config.yml</code>: Configuration file for setting paths.</li> </ul>
DYNA: Disease-Specific Language Model for Variant Pathogenicity
<p>For coding variant effect predictions (VEPs), our approach centers on clinical variant sets specifically related to inherited cardiomyopathies (CM) and arrhythmias (ARM). We utilize a pre-compiled dataset comprised of rare missense pathogenic and benign variants, categorized using a cohort-based approach for diseases such as cardiomyopathy and arrhythmias, as detailed in the previous report by Zhang et al. ClinVar CM and ARM datasets include all missense variants in CM and ARM, respectively, are extracted from ClinVar (Landrum et al.). In the realm of non-coding VEPs, our focus shifts to splicing-related variants, utilizing a dataset from the multiplexed assay for exon recognition by Chong et al., which highlights the significant impact of rare genetic variants on splicing disruptions. Similarly, the ClinVar Splicing dataset, compiled from ClinVar, encompasses all benign sequences and pathogenic variants pertinent to splicing.</p> <p> </p> <p>For the ClinVar CM and ARM datasets, we translate the DNA sequences into protein sequences using the human genome assembly hg38 from https://www.ncbi.nlm.nih.gov/grc/human. We employed the GFF file, MANE.GRCh38.v1.1.ensembl\_genomic.gff.gz from https://www.ncbi.nlm.nih.gov/refseq/MANE, to annotate coding versus non-coding regions for each gene, as only coding DNA sequences are translated into proteins. Additionally, protein domains, cataloged in the Pfam database (Finn et al.), are essential for the functional characterization of proteins. These domains are identified by aligning the translated sequences to known domain structures, thereby facilitating deeper insights into protein function.</p> <p> </p>
Data for "Deep learning-based model for diagnosing Alzheimer's disease and tauopathies"
<p>Image datasets and tuned models used in the paper (Koga et al., 2021). Data.zip contains image and text files for training models. Test.zip contains 12 images from 4 patients, which are a part of the hold-out dataset images used in the paper. There are 9 CSV files, which contain the results of tau burden quantification. Python code is available at GitHub (<a href="https://github.com/Koga-MD/DL-Tauopathies">https://github.com/Koga-MD/DL-Tauopathies</a>). </p>
ScienceDex guides
Understand access before you commit
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.