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3,476 results for “Parkinsons Disease”
Preventing Levodopa Induced Dyskinesia in Parkinson's Disease With HMG-CoA Reductase Inhibitors
ClinicalTrials.gov study NCT04064294. IPD Sharing: YES. Countries: 1. Publications: 3.
A Study of TAK-071 in People With Parkinson Disease
ClinicalTrials.gov study NCT04334317. IPD Sharing: YES. Countries: 1. Publications: 1.
Follow Up Study for Treatment of Parkinson's Disease With Deep Brain Stimulation
ClinicalTrials.gov study NCT01022073. IPD Sharing: UNDECIDED. Countries: 1. Publications: 1.
A Phase 3 Study of TVP-1012 (1 mg) in Early Parkinson's Disease Patients
ClinicalTrials.gov study NCT02337725. IPD Sharing: YES. Countries: 1. Publications: 1.
Data for: Developmental origins of Parkinson’s disease risk: perinatal exposure to the organochlorine pesticide dieldrin leads to sex-specific DNA modifications in critical neurodevelopmental pathways in the mouse midbrain
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Data from: Single-cell peripheral immunoprofiling of Lewy body and Parkinson’s disease in a multi-site cohort
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Data from: Loss of primary cilia and dopaminergic neuroprotection in pathogenic LRRK2driven and idiopathic Parkinson’s disease
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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>
Apresentação para Sessão Oral - CBEB2020: Evaluation of the Motor Performance of People with Parkinson's Disease through the Autocorrelation Function Estimated from Sinusoidal Drawings
<p>The objective of this work was to use the autocorrelation function to assess the fine motor performance of a healthy control group (CG) and people with Parkinson's disease (PD), whose fluctuations caused by the disease compromise motor skills, performed mainly by the hands and fingers essential for daily activities such as dressing, carrying objects and taking care of personal hygiene. For this, accelerometer signals were collected while the volunteers drew a sinusoidal pattern. The correlogram was estimated and two features were calculated from it: (i) the normalized area under the curve (𝑨𝒖𝑪); (ii) the difference between matching peaks and valleys from the reference and estimated correlograms (𝒗𝒎𝒎). These features allowed for the discrimination between drawing patterns of CG (𝒗𝒎𝒎= 0.154±0.063, 𝑨𝒖𝑪 = 0.204±0.040) and PD (𝒗𝒎𝒎 = 0.239±0.085, 𝑨𝒖𝑪 = 0.179±0.033) groups. Following the verification of normality (Shapiro-Wilk, p > 0.05), the t-test was applied to confirm the significant differences between groups (p < 0.05). The Cohen’s d effect size (p < 0.05) was medium (0.730) for 𝑨𝒖𝑪 and large (1.252) for 𝒗𝒎𝒎. This further confirms the differences between the features extracted from the groups. Therefore, the features 𝑨𝒖𝑪 and 𝒗𝒎𝒎 estimated from the autocorrelation function are effective for the assessment of the motor performance of healthy individuals and people with PD. </p>
Apresentação para o Prêmio Iniciação Científica - CBEB2020: Evaluation of the Motor Performance of People with Parkinson's Disease through the Autocorrelation Function Estimated from Sinusoidal Drawings
<p>The objective of this work was to use the autocorrelation function to assess the fine motor performance of a healthy control group (CG) and people with Parkinson's disease (PD), whose fluctuations caused by the disease compromise motor skills, performed mainly by the hands and fingers essential for daily activities such as dressing, carrying objects and taking care of personal hygiene. For this, accelerometer signals were collected while the volunteers drew a sinusoidal pattern. The correlogram was estimated and two features were calculated from it: (i) the normalized area under the curve (𝑨𝒖𝑪); (ii) the difference between matching peaks and valleys from the reference and estimated correlograms (𝒗𝒎𝒎). These features allowed for the discrimination between drawing patterns of CG (𝒗𝒎𝒎= 0.154±0.063, 𝑨𝒖𝑪 = 0.204±0.040) and PD (𝒗𝒎𝒎 = 0.239±0.085, 𝑨𝒖𝑪 = 0.179±0.033) groups. Following the verification of normality (Shapiro-Wilk, p > 0.05), the t-test was applied to confirm the significant differences between groups (p < 0.05). The Cohen’s d effect size (p < 0.05) was medium (0.730) for 𝑨𝒖𝑪 and large (1.252) for 𝒗𝒎𝒎. This further confirms the differences between the features extracted from the groups. Therefore, the features 𝑨𝒖𝑪 and 𝒗𝒎𝒎 estimated from the autocorrelation function are effective for the assessment of the motor performance of healthy individuals and people with PD. </p>
Data from: Developmental Dieldrin exposure alters DNA methylation at genes related to dopaminergic neuron development and Parkinson's disease in mouse midbrain
Human and animal studies have shown that exposure to the organochlorine pesticide dieldrin is associated with increased risk of Parkinson's disease (PD). Despite previous work showing a link between developmental dieldrin exposure and increased neuronal susceptibility to MPTP toxicity in male C57BL/6 mice, the mechanism mediating this effect has not been identified. Here, we tested the hypothesis that developmental exposure to dieldrin increases neuronal susceptibility via genome-wide changes in DNA methylation. Starting at 8 weeks of age and prior to mating, female C57BL/6 mice were exposed to 0.3 mg/kg dieldrin by feeding (every 3 days) throughout breeding, gestation, and lactation. At 12 weeks of age, pups were sacrificed and ventral mesencephalon, containing primarily substantia nigra, were microdissected. DNA was isolated and dieldrin-related changes in DNA methylation were assessed via reduced representation bisulfite sequencing (RRBS). We identified significant, sex-specific differentially methylated CpGs (DMCs) and regions (DMRs) by developmental dieldrin exposure (FDRNr4a2 and Lmx1b genes, which are involved in dopaminergic neuron development and maintenance. Developmental dieldrin exposure had distinct effects on the male and female epigenome. Together, our data suggest that developmental dieldrin exposure establishes sex-specific poised epigenetic states early in life. These poised epigenomes may mediate sensitivity to subsequent toxic stimuli and contribute to the development of late-life neurodegenerative disease, including PD.
A blinded, controlled trial of objective measurement in Parkinson's disease
<p>Medical conditions with effective therapies are usually managed with objective measurement and therapeutic targets. Parkinson's disease has effective therapies, but continuous objective measurement has only recently become available. This blinded, controlled study examined whether management of Parkinson's disease was improved when clinical assessment and therapeutic decisions were aided by objective measurement. The primary endpoint was improvement in the Movement Disorder Society-United Parkinson's Disease Rating Scale's (MDS-UPDRS) Total Score. In one arm, objective measurement assisted doctors to alter therapy over successive visits until objective measurement scores were in target. Patients in the other arm were conventionally assessed and therapies were changed until judged optimal. There were 75 subjects in the objective measurement arm and 79 in the arm with conventional assessment and treatment. There were statistically significant improvements in the moderate clinically meaningful range in the MDS-UPDRS Total, III, IV scales in the arm using objective measurement, but not in the conventionally treated arm. These findings show that global motor and non-motor disability is improved when the management of Parkinson's disease is assisted by objective measurement.</p>
PINK1 deficiency rewires early immune responses in a mouse model of Parkinson's disease triggered by intestinal infection
<p>Parkinson’s disease is characterized by a period of non-motor symptoms, including gastrointestinal dysfunction, preceding motor deficits by decades. This long prodrome is suggestive of peripheral immunity involvement in the initiation of disease. We previously developed a model system in PINK1 KO mice displaying PD-like motor symptoms at late stages following intestinal infections. Herein, we map the initiating immune events at the site of infection in this model. Using single-cell RNAseq, we demonstrate that peripheral myeloid cells are the earliest highly dysregulated immune cell type in PINK1 KO infected mice followed by an aberrant T cell response shortly after. We elucidate an increased propensity for antigen presentation mediated by myeloid-CD8+ T cell interaction. PINK1 KO activated myeloid cells acquire a proinflammatory profile inducing cytotoxic T cell responses. Together, our study provides the first evidence that PINK1 is a key regulator of immune functions in the gut underlying early PD-related disease mechanisms.</p>
Genome-wide meta-analysis of short-tandem repeats for Parkinson's disease risk
<p>Idiopathic Parkinson's disease (PD) is the second most common neurodegenerative disease after Alzheimer's disease and is determined by a combination of genetic and environmental risk factors. The to date largest genome-wide association study (GWAS) on single nucleotide polymorphisms (SNPs) by Nalls at al., 2019, reported 90 SNPs that were independently associated with PD risk. However, common SNPs account only for 16-36% of the total genetic heritability of the disease suggesting that other genetic variants play a role in PD susceptibility. One example of previously understudied genetic variants are short-tandem repeats (STR, also known as microsatellites), i.e., repeating sequence motifs in the human genome of 1-6 nucleotides in length. Thus, in this study, we performed a GWAS on imputed STRs in a large PD case-control dataset (n=4,757), and meta-analyzed these data with those from a previous study of the International PD Genetics Consortium (Bustos et al., 2023) resulting in a total sample size of 43,844 PD cases and controls. Thus, in this study, we performed a GWAS on imputed STRs in a large PD case-control dataset (n=4,757) from the US (the PEG and a GHC-based study) and Denmark (PASIDA).</p>
Enhanced mTORC1 signaling and protein synthesis in pathologic alpha-synuclein cellular and animal models of Parkinson's disease
<p>Pathologic alpha-synuclein plays an important role in the pathogenesis of alpha-synucleinopathies such as Parkinson's disease (PD). Disruption of proteostasis is thought to be central to pathologic alpha-synuclein (alpha-syn) toxicity; however, the molecular mechanism of this deregulation is poorly understood. Here we report that pathologic alpha-syn activates the mechanistic target of rapamycin (mTOR) complex 1 (mTORC1) leading to enhanced mRNA translation via binding tuberous sclerosis protein (TSC) 2 and destabilizing the TSC1-TSC2 complex. Genetic and pharmacologic inhibition of mTOR and protein synthesis rescue the dopamine neuron loss, behavioral deficits, and aberrant biochemical signaling in the alpha-syn preformed fibril (PFF) and Drosophila alpha-syn transgenic models of pathologic alpha-syn induced degeneration. Our findings establish a potential molecular mechanism by which pathologic alpha-syn activates mTORC1 leading to enhanced protein synthesis and concomitant neurodegeneration in PD.</p>
Oscillatory vs. non-oscillatory subthalamic beta activity in Parkinson's disease [Dataset]
<p>This datasets contain the subthalamic local field potentials (LFPs) from 21 Parkinson's disease patients, used in the work "Oscillatory vs. non-oscillatory subthalamic beta activity in Parkinson's disease". Subthalamic LFPs are stored in MATLAB format (.mat). Further information on patients can be found in the main article.</p>
A potential patient stratification biomarker for Parkinson´s disease based on LRRK2 kinase-mediated centrosomal alterations in peripheral blood-derived cells
<p>Annotated WES VCF file and phenotype file used in Gene burden analysis of Naaldijk et al., "A potential patient stratification biomarker for Parkinson´s disease based on LRRK2 kinase-mediated centrosomal alterations in peripheral blood-derived cells", 2023. </p><p> </p>
Articulatory features of plosive consonants for early detection of Parkinson's disease
<p>These datasets contain temporal and spectral features extracted from the Voice Onset Time (VOT) segments of /p/, /t/ and /k/ syllables for a audio database composed of 27 individuals diagnosed with PD and 27 healthy controls. Data are presented both in CSV and Excel formats.</p> <p>These datasets have been created and used in a full computer-aided diagnosis system. All information about the feature extraction process is presented in:</p> <p>David Montaña, Yolanda Campos-Roca, Carlos J. Pérez, A Diadochokinesis-based expert system considering articulatory features of plosive consonants for early detection of Parkinson’s disease, Computer Methods and Programs in Biomedicine, Volume 154, 2018, 89-97, ISSN: 0169-2607, DOI: 10.1016/j.cmpb.2017.11.010.</p> <p> </p> <p> </p>
Voxel-wise maps for the paper: Longitudinal associations of magnetic susceptibility with clinical severity in Parkinson's disease
<p>This upload contains voxel-wise group level QSM data, and statistical maps for group level results associated with the paper: Longitudinal associations of magnetic susceptibility with clinical severity in Parkinson's disease.</p> <p>The assocaited code for reproducing these statistical maps can be found here: <a href="https://github.com/gecthomas/QSM_PD_longitudinal">gecthomas/QSM_PD_longitudinal (github.com)</a></p>
Extended data for behavioural change for Parkinson's disease: A randomised controlled feasibility study to promote physical activity and exercise adherence among people with Parkinson's, study protocol
<p><strong>Background: </strong>Parkinson's is a common progressive neurological condition characterized by motor and non-motor deficits. Physical activity and exercise can improve health, but many people with Parkinson's have trouble reaching the recommended dosage. Our recent literature review found improvements in exercise adherence with behavioural change interventions, but it remains unclear which are most effective. Further qualitative research and patient and public involvement has informed a novel behavioural change support intervention to be tested alongside an existing exercise program.<strong> </strong></p> <p><strong>Objective: </strong>To examine the feasibility of behavioural change support techniques delivered alongside an exercise programme to improve physical activity, function, and self-efficacy in PwP (and study procedures) to inform a future pilot RCT trial.<strong> </strong></p> <p><strong>Methods: </strong>A parallel-arm single blinded randomised feasibility study. Twenty participants with Parkinson's (Hoehn and Yahr stage 1-3) will be recruited from a physiotherapy primary-care waiting list. Following written consent, and baseline assessment, the participants will be randomly allocated to the intervention (n=10) or the control group (n=10). Both groups will receive usual care, which includes a weekly program of a multidisciplinary education, a supervised exercise class and a prescribed home exercise program. The intervention group will receive additional behavioural change techniques, targeting behaviour regulation, belief about capabilities and social influences. Class and home exercise adherence, behavioural component uptake and adherence, and negative events will be recorded. Outcomes will include enrolment and maintenance rates, physical function, falls, physical activity, and exercise self-efficacy measured pre- and post- the 12- week program (in-person). Surveys will be used to compare experiences and satisfaction between groups. Exit interviews will be completed with the intervention group only, exploring their experience of the behavioural change techniques. </p> <p><strong>Discussion: </strong>The results will help inform a future pilot RCT, based on the intervention acceptability, consent rate, maintenance, and protocol integrity.</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.