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.
3,900
datasets available to search
ShareScore release 0.9.0
Dataset results
3,900 results for “parkinsonism”
Barriers to home exercise for patients with Parkinson's disease – a qualitative study
<p><strong>Objective</strong>: This study aimed to explore the barriers to home exercise for patients with Parkinson's disease (PwPDs) and provide guidelines for healthcare providers (HcPs) to build and implement home exercise strategies for PwPDs.</p> <p><strong>Design</strong>: A qualitative descriptive method was used. Semi-structured interviews were conducted and thematic analysis was employed.</p> <p><strong>Setting</strong>: The study was conducted in the Department of Neurology at a Grade 3 Class A general hospital in China.</p> <p><strong>Participants</strong>: A total of 22 participants were interviewed, including 10 PwPDs, seven caregivers, two nurses, one head nurse, and two Parkinson's clinicians.</p> <p><strong>Results</strong>: Five themes were identified in this analysis. (1) Psychosomatic stress and low activity; (2) lack of early rehabilitation authorisation; (3) poor "flow" state of home exercise; (4) inaccessibility of continued service; (5) sociocultural impact on family coping.</p> <p><strong>Conclusion</strong>: PwPDs, caregivers, and specialised medical staff raised the challenges faced by patients' home exercises from different perspectives. Interventions can improve services and integrate resources through the management of multi-disciplinary, early rehabilitation authorisation, exercise experience, continuous service mode, and family coping strategies under different cultures to gradually adjust the home exercise behaviour of PwPDs.</p>
Datset related to article: "ACTB gene mutation in combined Dystonia-Deafness syndrome with parkinsonism: Expanding the phenotype and highlighting the long-term GPi DBS outcome"
<p>Sanger sequences (.abi files) validating variants found with whole exome sequencing</p>
Data for: Deep brain stimulation in early-stage Parkinson disease
<p><strong>Objective</strong>: To report 5-year outcomes from the subthalamic nucleus (STN) deep brain stimulation (DBS) in early-stage Parkinson disease (PD) pilot clinical trial.</p> <p><strong>Methods</strong>: The pilot was a prospective, single-blind clinical trial that randomized patients with early-stage PD (Hoehn & Yahr II off medications) to receive bilateral STN DBS plus optimal drug therapy (ODT) vs ODT alone (IDEG050016, NCT0282152, IRB040797). Participants who completed the 2-year trial participated in this observational follow-up study, which included annual outpatient visits through 5 years. This analysis includes 28 patients who were taking PD medications for 6 months to 4 years at enrollment. Outcomes were analyzed using both proportional odds logistic regression and linear mixed effects models.ResultsEarly STN DBS + ODT participants required lower levodopa equivalent daily doses (p = 0.04, β = −240 mg, 95% confidence interval [CI] −471 to −8) and had 0.06 times the odds of requiring polypharmacy at 5 years compared to early ODT participants (p = 0.01, odds ratio [OR] 0.06, 95% CI 0.00 to 0.65). The odds of having worse rest tremor for early STN DBS + ODT participants were 0.21 times those of early ODT participants (p < 0.001, OR 0.21, 95% CI 0.09 to 0.45). The safety profile was similar between groups.</p> <p><strong>Conclusions</strong>: These results suggest that early DBS reduces the need for and complexity of PD medications while providing long-term motor benefit over standard medical therapy. Further investigation is warranted, and the Food and Drug Administration has approved the conduct of a prospective, multicenter, pivotal clinical trial of DBS in early-stage PD (IDEG050016).</p> <p><strong>Classification of evidence</strong>: This study provides Class II evidence that DBS implanted in early-stage PD decreases the risk of disease progression and polypharmacy compared to optimal medical therapy alone.</p>
Protein network analysis links the NSL complex to Parkinson's disease via mitochondrial & nuclear biology
<p>This online depository corresponds to manuscript : <em>Protein network analysis links the NSL complex to Parkinson’s disease via mitochondrial & nuclear biology.</em></p> <p><strong>Authors: </strong><em>Katie Kelly, Patrick A. Lewis, Helene Plun-Favreau, Claudia Manzoni</em></p> <p>Whilst the majority (~90-95%) of PD cases are sporadic, much of our understanding of the pathophysiological basis of disease can be traced back to the study of rare, monogenic forms of disease. However, in the past decade, the availability of Genome-Wide Association Studies (GWAS) has facilitated a shift in focus, toward identifying common risk variants conferring an increased risk of developing PD across the population. </p> <p>A recently developed mitophagy screening assay of GWAS candidates, has functionally implicated the non-specific lethal (NSL) complex, a chromatin remodeler, in the regulation of PINK1-mitophagy. Here, a bioinformatics approach has been taken to investigate the interactome of the NSL complex, to unpick its relevance to PD progression. The mitochondrial interactome of the NSL complex has been built, mining 3 separate repositories: PINOT, HIPPIE and MIST, for curated, literature-derived protein-protein interaction (PPI) data. A multi-layered approach has been taken to; i) build the ‘mitochondrial’ NSL interactome, applying PD gene-set enrichment analysis to explore the relevance of the NSL mitochondrial interactome to PD and, ii) build the PD-oriented NSL interactome, using functional enrichment, to uncover biological pathways underpinning the NSL /PD association.</p>
Parkin regulates amino acid homeostasis at mitochondria-lysosome (M/L) contact sites in Parkinson's disease
<p>Mutations in the E3 ubiquitin ligase parkin are the most common cause of early-onset Parkinson's disease (PD). Although parkin modulates mitochondrial and endolysosomal homeostasis during cellular stress, whether parkin regulates mitochondrial and lysosomal crosstalk under physiologic conditions remains unresolved. Using transcriptomics, metabolomics, and super-resolution microscopy, we identify amino acid metabolism as a disrupted pathway in iPSC-derived dopaminergic neurons from parkin PD patients. Compared to isogenic controls, parkin mutant neurons exhibit decreased mitochondria-lysosome contacts via destabilization of active Rab7. Subcellular metabolomics in parkin mutant neurons reveals amino acid accumulation in lysosomes and their deficiency in mitochondria. Knockdown of the Rab7 GTPase-activating protein TBC1D15 restores mitochondria-lysosome tethering and ameliorates cellular and subcellular amino acid profiles in parkin mutant neurons. Our data thus uncover a function of parkin in promoting mitochondrial and lysosomal amino acid homeostasis through stabilization of mitochondria-lysosome contacts and suggest that modulation of inter-organelle contacts may serve as a potential target for ameliorating amino acid dyshomeostasis in disease.</p>
A five-sensor IMU-based Parkinson's disease patient and control dataset including three activities of daily living
<p class="MsoNormal">Parkinson's disease is an often-debilitating progressive neurological condition leading to loss of motor control. This dataset contains kinematic sensor data from two groups: one containing 15 patients with Parkinson's disease, and a control group of 19 participants without any known neurological condition. Participant ages ranged from 40–85, 21 were male, and 13 were female. The participants wore five 9-axis Inertial Measurement Units (IMUs) – one on each upper arm, each lower arm, and on their head. They were asked to perform a calibration pose, followed by three activities: making toast, putting on a cardigan, and unlocking and opening a door, with each activity repeated three times. The IMUs recorded time-series acceleration and orientation data from the moment where the participant was instructed to begin the activity (inception of the idea to act), through to the activity's completion. This dataset is planned for use in intent-sensing studies for assistive device control but is also applicable for activity recognition.</p>
Data from: Developmental exposure to the Parkinson's disease-associated organochlorine pesticide dieldrin alters dopamine neurotransmission in α-synuclein pre-formed fibril (PFF)-injected mice
<p>Parkinson's disease (PD) is the fastest-growing neurological diseases worldwide, with increases outpacing aging and most rapid in recently industrialized areas, suggesting the role of environmental factors. Together, epidemiological studies, post-mortem analysis and mechanistic studies suggest that exposure to persistent organic pollutants, including the organochlorine pesticide dieldrin, increases PD risk. In mouse models, developmental dieldrin exposure causes male-specific exacerbation of neuronal susceptibility to MPTP and synucleinopathy. Specifically, developmental dieldrin exposure induces male-specific exacerbation of toxicity in the α-synuclein (α-syn) pre-formed fibril (PFF) model with increased deficits in striatal dopamine (DA) turnover and motor deficits on the challenging beam. Here, we hypothesized that alterations in DA handling contribute to the observed changes and assessed vesicular monoamine transporter 2 (VMAT2) function and DA release in this dieldrin/PFF two-hit model. Female C57BL/6 mice were exposed to 0.3 mg/kg dieldrin or vehicle every 3 days by feeding, starting at 8 weeks of age by ingestion and continuing throughout breeding, gestation, and lactation. Male offspring from independent litters underwent unilateral, intrastriatal injections of α-syn PFFs at 12 weeks of age and vesicular <sup>3</sup>H-DA uptake assays and fast-scan cyclic voltammetry (FSCV) were performed at 4 months post-PFF injection. We observed a dieldrin-induced increase in DA release in striatal slices in PFF-injected animals, but no change in VMAT2 activity. These results suggest that developmental dieldrin exposure increases a compensatory response to synucleinopathy-triggered striatal DA loss and supports our hypothesis that alterations in DA handling may underly the observed exacerbation of PFF-induced deficits in motor behavior and DA turnover.</p>
Assessing the Maturity level of Wearable Sensors for Home Monitoring in Parkinson's Disease through Evidence Evaluation Levels (EEL) and User Experience: A Comprehensive Review
<p>Source files for the PRISMA diagram and Figure 1 of the comprehensive review: Assessing the Maturity level of Wearable Sensors for Home Monitoring in Parkinson’s Disease through Evidence Evaluation Levels (EEL) and User Experience</p>
Support for Physical Activity in Everyday Life With Parkinson's Disease
ClinicalTrials.gov study NCT05510739. IPD Sharing: NO. Countries: 1. Publications: 1.
PF-06669571 In Subjects With Idiopathic Parkinson's Disease
ClinicalTrials.gov study NCT02565628. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Study of Parkinson's Early Stage With Deferiprone
ClinicalTrials.gov study NCT02728843. IPD Sharing: NO. Countries: 4. Publications: 1.
Evaluating the Efficacy, Safety, Pharmacokinetics, and Pharmacodynamics of BIIB054 in Participants With Parkinson's Disease
ClinicalTrials.gov study NCT03318523. IPD Sharing: YES. Countries: 9. Publications: 3.
A Study To Evaluate The Safety And Efficacy Of IPX066 In Advanced Parkinson's Disease (ADVANCE-PD).
ClinicalTrials.gov study NCT00974974. IPD Sharing: NO. Countries: 8. Publications: 2.
Kick Out Parkinson's Disease 2
ClinicalTrials.gov study NCT03882879. IPD Sharing: Not stated. Countries: 1. Publications: 2.
Physical Therapy and Deep Brain Stimulation in Parkinson Disease
ClinicalTrials.gov study NCT03181282. IPD Sharing: NO. Countries: 1. Publications: 1.
Repetitive Transcranial Magnetic Stimulation for Musculoskeletal Pain in Patients With Parkinson's Disease
ClinicalTrials.gov study NCT05537597. IPD Sharing: NO. Countries: 1. Publications: 6.
Coping With Depression in Parkinson's Disease
ClinicalTrials.gov study NCT00464464. IPD Sharing: Not stated. Countries: 1. Publications: 6.
A Study of LY3154207 in Participants With Dementia Due to Lewy Body Dementia (LBD) Associated With Idiopathic Parkinson's Disease (PD) or Dementia With Lewy Bodies (DLB)
ClinicalTrials.gov study NCT03305809. IPD Sharing: YES. Countries: 3. Publications: 2.
Clinical Trial of Apomorphine Subcutaneous Infusion in Patients With Advanced Parkinson's Disease
ClinicalTrials.gov study NCT02006121. IPD Sharing: NO. Countries: 7. Publications: 2.
Pramipexole Versus Placebo in Parkinson's Disease (PD) Patients With Depressive Symptoms
ClinicalTrials.gov study NCT00297778. IPD Sharing: Not stated. Countries: 13. Publications: 1.
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.