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341
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ShareScore release 0.9.0
Dataset results
341 results for “Neurodegeneration”
Effects of Ozanimod on Immune-mediated Mechanisms of Neurodegeneration in Multiple Sclerosis - a Preclinical Study
ClinicalTrials.gov study NCT05245344. IPD Sharing: NO. Countries: 1. Publications: 32.
Evaluation of the Role of Neurodegeneration in Schizophrenia
ClinicalTrials.gov study NCT05257720. IPD Sharing: NO. Countries: 1. Publications: 11.
Longitudinal Evaluation of Amyloid Risk and Neurodegeneration - the LEARN Study
ClinicalTrials.gov study NCT02488720. IPD Sharing: Not stated. Countries: 1. Publications: 7.
Metformin Add-on Clinical Study in Multiple Sclerosis to Evaluate Brain Remyelination And Neurodegeneration
ClinicalTrials.gov study NCT05893225. IPD Sharing: YES. Countries: 1. Publications: 1.
Tracking Neurodegeneration in Early Wolfram Syndrome
ClinicalTrials.gov study NCT02455414. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Genes, Exercise, Memory and Neurodegeneration
ClinicalTrials.gov study NCT01021644. IPD Sharing: Not stated. Countries: 1. Publications: 5.
Biomarker Exploration in Aging, Cognition and Neurodegeneration
ClinicalTrials.gov study NCT03860857. IPD Sharing: NO. Countries: 1. Publications: 5.
Retinal Neurodegeneration in Type 2 Diabetes as Biomarker for Alzheimer´s Disease
ClinicalTrials.gov study NCT02360527. IPD Sharing: NO. Countries: 1. Publications: 1.
Alemtuzumab in Autoimmune Inflammatory Neurodegeneration: Mechanisms of Action and Neuroprotective Potential
ClinicalTrials.gov study NCT02419378. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Study of Axial and Cognitive Symptoms and Biomarkers of Neurodegeneration in Brain-first and Body-first PD
ClinicalTrials.gov study NCT07187843. IPD Sharing: UNDECIDED. Countries: 1. Publications: 6.
Exploring the Utility of [18F]3F4AP for Demyelination Imaging in Controls, Neurodegeneration and Traumatic Brian Injury
ClinicalTrials.gov study NCT04710550. IPD Sharing: NO. Countries: 1. Publications: 1.
Self-Care Training for Family Caregivers of Persons With Neurodegeneration
ClinicalTrials.gov study NCT06200909. IPD Sharing: NO. Countries: 1. Publications: 5.
CSF synaptic biomarkers in the preclinical stage of Alzheimer's disease and their association with MRI and PET markers of neurodegeneration: a cross-sectional study
<p>Objective: To determine whether CSF synaptic biomarkers are altered in the early preclinical stage of the Alzheimer's <i>continuum</i> and associated with Alzheimer's disease (AD) risk factors, primary pathology, and neurodegeneration markers.</p> <p>Methods: Cross-sectional study in the ALFA+ cohort, comprising middle-aged cognitively unimpaired participants. CSF neurogranin and GAP-43 were measured using immunoassays and SNAP-25 and synaptotagmin-1 using immunoprecipitation mass spectrometry. AD CSF biomarkers Aβ42/40, p-tau and t-tau, and the neurodegeneration biomarker NfL were also measured. Participants underwent structural MRI, and <span>fluorodeoxyglucose and</span> Aβ<span> PET imaging. General linear modeling was used to test the associations between CSF synaptic biomarkers and risk factors, </span>Aβ<span> pathology, tau pathology, and neurodegeneration markers.</span></p> <p>Results: All CSF synaptic biomarkers increased with age. CSF neurogranin was higher in females, while CSF SNAP-25 was higher in <i>APOE-</i>ε4 carriers. All CSF synaptic biomarkers increased with higher Aβ load (as measured by CSF Aβ42/40 and Aβ PET Centiloid values) and, importantly, the synaptic biomarkers were increased even in individuals in the earliest stages of Aβ deposition. Higher CSF synaptic biomarkers were also associated with higher CSF p-tau and NfL. Higher CSF neurogranin and GAP-43 were significantly associated with higher brain metabolism, but lower cortical thickness in AD-related brain regions.</p> <p>Conclusion: CSF synaptic biomarkers increase in early preclinical stages of the Alzheimer's <i>continuum </i>even when a low burden of Aβ pathology is present, and they differ in their association with age, sex, <i>APOE-</i>ε4<i>,</i> and markers of neurodegeneration.</p>
Parkinson's disease-related brain metabolic patterns and neurodegeneration in isolated REM sleep behavior disorder
<p><span><b>Objective</b>: To elucidate the role of Parkinson's disease (PD)-related brain metabolic patterns as a biomarker in isolated rapid-eye-movement sleep behavior disorder (iRBD) for future disease conversion.</span></p> <p><span><b>Method</b>: This is a prospective cohort study consisting of 30 iRBD patients, 25 de novo PD patients with a premorbid history of RBD, 21 long-standing PD patients on stable treatment and 24 healthy controls. iRBD group was longitudinally followed up. All participants underwent <sup>18</sup>F-Fluorodeoxyglucose (FDG) PET and were evaluated with olfaction, cognition, and the Movement disorders society-Unified PD Rating Scale (MDS-UPDRS) at baseline. From FDG-PET scans, we derived metabolic patterns from the long-standing PD group (PD-RP) and de novo PD group with RBD (dnPDRBD-RP). Subsequently, we calculated the PD-RP and dnPDRBD-RP scores in iRBD patients. We validated the metabolic patterns in each PD group and separate iRBD cohort (<i>n</i>=14).</span></p> <p><span><b>Result</b>: The two patterns significantly correlated with each other and were spatially overlapping yet distinct. The MDS-UPDRS motor scores significantly correlated with PD-RP (<i>p</i> = 0.013) but not with dnPDRBD-RP (<i>p</i> = 0.076). In contrast, dnPDRBD-RP correlated with olfaction in butanol threshold test (<i>p</i> = 0.018) in iRBD subjects, but PD-RP did not (<i>p</i> = 0.21). High dnPDRBD-RP in iRBD patients predicted future phenoconversion with all cut-off ranges from 1.5 to 3 standard deviations of the control value, whereas predictability of PD-RP was only significant in a partial range of cut-off.</span></p> <p><b>Conclusion:</b> The dnPDRBD-RP is an efficient neuroimaging biomarker that reflects prodromal features of PD and predicts phenoconversion in iRBD that can be applied individually.</p>
Association of aortic stiffness with biomarkers of neuroinflammation, synaptic dysfunction, and neurodegeneration
<p><b>Objectives:</b> To test the hypothesis that increased aortic stiffening is associated with greater cerebrospinal fluid (CSF) evidence of core Alzheimer's disease pathology (Ab, phosphorylated tau (p-tau)), neurodegeneration (total tau (t-tau)), synaptic dysfunction (neurogranin), neuroaxonal injury (neurofilament light (NFL)), and neuroinflammation (YKL-40, sTREM2), we analyzed pulse wave velocity (PWV) data and CSF data among older adults.</p> <p><b>Methods: </b>Participants free of stroke and dementia from the Vanderbilt Memory and Aging Project, an observational community-based study, underwent cardiac magnetic resonance to assess aortic pulse wave velocity (PWV, m/sec) and lumbar puncture to obtain CSF. Linear regressions related aortic PWV to CSF Ab, p-tau, t-tau, neurogranin, NFL, YKL-40, and sTREM2 concentrations adjusting for age, race/ethnicity, education, apolipoprotein (<i>APOE</i>) e4 status, Framingham Stroke Risk Profile, and cognitive diagnosis. Models were repeated testing PWV interactions with age, diagnosis, <i>APOE</i>-e4, and hypertension on each biomarker.</p> <p><strong>Results:</strong> 146 participants were examined (72±6 years). Aortic PWV interacted with age on p-tau (b=0.31, p=0.04), t-tau, (b=2.67, p=0.05), neurogranin (b=0.94, p=0.04), and sTREM2 (b=20.4, p=0.05). Among participants over age 73 years, higher aortic PWV related to higher p-tau (b=2.4, p=0.03), t-tau (b=19.3, p=0.05), neurogranin (b=8.4, p=0.01), and YKL-40 concentrations (b=7880, p=0.005). Aortic PWV had modest interactions with diagnosis on neurogranin (b=-10.76, p=0.03) and hypertension status on YKL-40 (b=-18020, p<0.001).</p> <p><b>Conclusions:</b> Among our oldest participants, age 74 years and older, greater aortic stiffening is associated with <i>in vivo</i> biomarker evidence of neuroinflammation, tau phosphorylation, synaptic dysfunction, and neurodegeneration, but not amyloidosis. Central arterial stiffening may lead to cumulative cerebral microcirculatory damage and blood flow delivery to tissue, resulting in neuroinflammation and neurodegeneration in more advanced age.</p>
Data from: Biallelic SQSTM1 mutations in early-onset, variably progressive neurodegeneration
Objective: To characterize clinically and molecularly an early-onset, variably progressive neurodegenerative disorder characterized by a cerebellar syndrome with severe ataxia, gaze palsy, dyskinesia, dystonia, and cognitive decline affecting 11 individuals from 3 consanguineous families. Methods: We used whole-exome sequencing (WES) (families 1 and 2) and a combined approach based on homozygosity mapping and WES (family 3). We performed in vitro studies to explore the effect of the nontruncating SQSTM1 mutation on protein function and the effect of impaired SQSTM1 function on autophagy. We analyzed the consequences of sqstm1 down-modulation on the structural integrity of the cerebellum in vivo using zebrafish as a model. Results: We identified 3 homozygous inactivating variants, including a splice site substitution (c.301+2T>A) causing aberrant transcript processing and accelerated degradation of a resulting protein lacking exon 2, as well as 2 truncating changes (c.875_876insT and c.934_936delinsTGA). We show that loss of SQSTM1 causes impaired production of ubiquitin-positive protein aggregates in response to misfolded protein stress and decelerated autophagic flux. The consequences of sqstm1 down-modulation on the structural integrity of the cerebellum in zebrafish documented a variable but reproducible phenotype characterized by cerebellum anomalies ranging from depletion of axonal connections to complete atrophy. We provide a detailed clinical characterization of the disorder; the natural history is reported for 2 siblings who have been followed up for >20 years. Conclusions: This study offers an accurate clinical characterization of this recently recognized neurodegenerative disorder caused by biallelic inactivating mutations in SQSTM1 and links this phenotype to defective selective autophagy.
Hypertension, Brain Clearance, and Markers of Neurodegeneration
ClinicalTrials.gov study NCT05785871. IPD Sharing: YES. Countries: 1. Publications: 0.
Effect of Fingolimod on Neurodegeneration
ClinicalTrials.gov study NCT02575365. IPD Sharing: NO. Countries: 1. Publications: 0.
Retinal Neurodegeneration In Type 2 Diabetes Mellitus Detected by Optical Coherence Tomography
ClinicalTrials.gov study NCT04808804. IPD Sharing: Not stated. Countries: 0. Publications: 13.
Tysabri Effects on Cognition and Neurodegeneration in Multiple Sclerosis
ClinicalTrials.gov study NCT01071512. IPD Sharing: Not stated. Countries: 1. Publications: 0.
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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.