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872
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ShareScore release 0.9.0
Dataset results
872 results for “disease progression”
A multiomics disease progression signature of low-risk ccRCC
GEO Series GSE207557. Homo sapiens. 24 samples. Type: Non-coding RNA profiling by high throughput sequencing.
Effect of prexasertib on disease progression and survival in High grade serous ovarian cancer patients
GEO Series GSE149723. Homo sapiens. 30 samples. Type: Expression profiling by high throughput sequencing.
Prolonged Glucagon Exposure Rewires Lipid Oxidation and Drives Diabetic Kidney Disease Progression
GEO Series GSE253774. Mus musculus. 17 samples. Type: Expression profiling by high throughput sequencing.
PLN tissue- and age-specific changes in gene expression during disease induction and progression in NOD mice.
GEO Series GSE15150. Mus musculus. 35 samples. Type: Expression profiling by array.
Distinct effects of restricting individual branched-chain amino acids on the development and progression of Alzheimer’s disease in 3xTg mice
GEO Series GSE299928. Mus musculus. 47 samples. Type: Expression profiling by high throughput sequencing.
Genome-wide CRISPR/Cas9 library screening identified OGDH as a regulator of disease progress and HMAs-resistance in MDS by reprogramming glutamine metabolism
GEO Series GSE273914. Homo sapiens. 5 samples. Type: Other.
Connexin 30 deficiency ameliorates the disease progression of amyotrophic lateral sclerosis model mice by suppressing glial inflammation.
GEO Series GSE213844. Mus musculus. 3 samples. Type: Expression profiling by array.
Identifying urinary RNA as non-invasive biomarkers for progression of chronic kidney disease
GEO Series GSE121978. Homo sapiens. 80 samples. Type: Non-coding RNA profiling by high throughput sequencing.
Hepatic T-cell senescence is implicated in the progression of fatty liver disease in patients with type 2 diabetes
GEO Series GSE239612. Mus musculus. 2 samples. Type: Expression profiling by high throughput sequencing.
Data from: INTREPAD: a randomized trial of naproxen to slow progress of presymptomatic Alzheimer disease
Objective: Evaluate the safety and efficacy of low-dose naproxen for prevention of progression in pre-symptomatic AD among cognitively intact persons at-risk. Methods: INTREPAD, a two-year double-masked pharmaco-prevention trial, enrolled 195 AD family history-positive elderly (mean age 63 years) screened carefully to exclude cognitive disorder. These were randomized 1:1 to naproxen sodium 220mg twice-daily or placebo. Multimodal imaging, neurosensory, cognitive and (in ~50%) CSF biomarker evaluations were performed at Baseline, 3, 12, and 24 months. A modified intent-to-treat analysis considered 160 participants who remained on-treatment through their first follow-up examination. The primary outcome was rate of change in a multimodal composite pre-symptomatic Alzheimer Progression Score (APS). Results: Safety: Naproxen-treated individuals showed a clear excess of adverse events. Efficacy: Among treatment groups combined, the APS increased by 0.101 points/year (S.E = 0.014; P < 10-5), but rate of change showed little difference by treatment assignment (0.017 points/year). The treatment-related slope ratio of 1.10 (95% Confidence Interval 0.588–2.04) suggested that naproxen does not reduce the rate of APS progression by more than 41%. Secondary analyses revealed no notable treatment effects on individual CSF, cognitive, or neurosensory biomarker indicators of progressive pre-symptomatic AD. Conclusions: In cognitively intact individuals at-risk, sustained treatment with naproxen sodium 220 mg twice-daily increases frequency of adverse health effects but does not reduce apparent progression of pre-symptomatic AD. Classification of Evidence: This study provides Class I evidence that, for people who are cognitively intact, low-dose naproxen does not significantly reduce progression of a composite indicator of pre-symptomatic AD.
Evolution of retinal degeneration and prediction of disease activity in relapsing and progressive multiple sclerosis
<p>Retinal optical coherence tomography has been identified as biomarker for disease progression in relapsing-remitting multiple sclerosis (RRMS), while the dynamics of retinal atrophy in progressive MS are less clear. We investigated retinal layer thickness changes in RRMS, primary and secondary progressive MS (PPMS, SPMS), and their prognostic value for disease activity.</p> <p>After quality control, 2651 OCT measurements of 195 RRMS, 87 SPMS, 125 PPMS patients, and 98 controls from five German MS centers were analyzed. Peripapillary and macular retinal nerve fiber layer (pRNFL, mRNFL) thickness predicted future relapses in all MS and RRMS patients without history of optic neuritis while mRNFL and ganglion cell-inner plexiform layer (GCIPL) thickness predicted future MRI progression/activity in RRMS without history of optic neuritis (mRNFL, GCIPL) and PPMS (GCIPL). mRNFL thickness predicted future disability progression in PPMS: However, thickness change rates were subject to considerable amounts of measurement variability.</p> <p>In conclusion, retinal degeneration, most pronounced of pRNFL and GCIPL, occurs in all subtypes. Using the current state of technology, longitudinal assessments of retinal thickness may not be suitable on a single patient level.</p>
Data from: Cognitive reserve and clinical progression in Alzheimer's disease: a paradoxical relationship
Objective: To investigate the relationship between cognitive reserve (CR) and clinical progression across the Alzheimer's disease (AD) spectrum. Methods: We selected 839 Aβ-positive subjects with normal cognition (NC, n=175), mild cognitive impairment (MCI, n=437) or AD dementia (n=227) from the Alzheimer's Disease Neuroimaging Initiative. CR was quantified using standardized residuals (W-scores) from a (covariate-adjusted) linear regression with global cognition (ADAS-Cog 13) as an independent variable-of-interest, and either gray matter volumes or white matter hyperintensity volume as dependent variables. These W-scores, reflecting whether an individual's degree of cerebral damage is lower or higher than clinically expected, were tested as predictors of diagnostic conversion (i.e. NC to MCI/AD dementia, or MCI to AD dementia) and longitudinal changes in memory (ADNI-MEM) and executive functions (ADNI-EF). Results: The median follow-up period was 24 months (interquartile range: 6-42). Corrected for age, sex, APOE4-status and baseline cerebral damage, higher gray matter volume-based W-scores (i.e. greater CR) were associated with a lower diagnostic conversion risk (hazard ratio [HR]= .22, p<.001) and slower decline in memory (β=.48, p<.001) and executive functions (β=.67, p<.001). Stratified by disease stage, we found similar results for NC (diagnostic conversion: HR=.30, p=.038; ADNI-MEM: β=.52, p=.028; ADNI-EF: β=.42, p=.077) and MCI (diagnostic conversion: HR=.21, p<.001; ADNI-MEM: β=.43, p=.003; ADNI-EF: β=.59, p<.001), but opposite findings (i.e. more rapid decline) for AD dementia (ADNI-MEM: β=-.91, p=.002; ADNI-EF: β=-.77, p=.081). Conclusions: Among Aβ-positive individuals, greater CR related to attenuated clinical progression in pre-dementia stages of AD, but accelerated cognitive decline after the onset of dementia.
Effect of 2.5 Years of Rasagiline Therapy on Progression of Cognitive Biomarkers Assessed by MRI in Parkinson's Disease.
ClinicalTrials.gov study NCT02278588. IPD Sharing: Not stated. Countries: 1. Publications: 0.
Social Medical Progression of Coronary Heart Disease With Associated Psychosocial Comorbidity -Interval Rehabilitation.
ClinicalTrials.gov study NCT01589536. IPD Sharing: Not stated. Countries: 1. Publications: 0.
A Prospective Study of Clinical Factors Affecting Disease Progression and Treatment Results of Patients With Tumors of the Prostate, Bladder and Kidney.
ClinicalTrials.gov study NCT02186925. IPD Sharing: Not stated. Countries: 1. Publications: 0.
Social-environmental, Psychosocial, Behavioral, Clinical and Biological Drivers of Disparities in Liver Disease Progression Among Korean American With Chronic Hepatitis B Infection
ClinicalTrials.gov study NCT05117541. IPD Sharing: Not stated. Countries: 1. Publications: 0.
Role of Statins In Slowing Rheumatic Heart Disease (RHD) Progression
ClinicalTrials.gov study NCT04575857. IPD Sharing: NO. Countries: 1. Publications: 0.
Ganagliflozin on the Progression of Kidney Disease in Subjects With Type 2 Diabetes Mellitus and Chronic Kidney Disease
ClinicalTrials.gov study NCT07116928. IPD Sharing: Not stated. Countries: 1. Publications: 0.
AI-based Progression and Medication Response Prediction Study in Parkinson's Disease
ClinicalTrials.gov study NCT07189468. IPD Sharing: NO. Countries: 4. Publications: 0.
Monitoring of Early Disease Progression in Hereditary Transthyretin Amyloidosis
ClinicalTrials.gov study NCT03431896. IPD Sharing: Not stated. Countries: 1. Publications: 0.
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.