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80 results for “Spinocerebellar ataxia”
Multi-omic Insights into Molecular Mechanism and Therapeutic Targets in Spinocerebellar Ataxia type 7
<p>The molecular mechanism in spinocerebellar ataxia type 7 is currently poorly understood. To provide understandings, a multi-omic study was performed using SCA7266Q/5Q mice. At week 12, entire brain tissue samples were collected and RNA sequencing, methylation analysis, and proteomic analysis were performed. Results were integrated to identify genes with identical trends in expression. Data was also compared with SCA patient serum proteomic analysis, and based on common differentially expressed proteins, a Naïve Bayesian network model was constructed to predict nilotinib treatment response. Data from RNA sequencing and methylation analysis revealed 58 significantly hypomethylated-upregulated genes and 62 hypermethylated-downregulated genes, mostly enriched in GO terms of regulation of axonogenesis, channel activity, and monoamine signaling. In the proteomic analysis, 211 upregulated and 281 downregulated DEPs associated mostly with immune response and cellular mobility were identified. Two genes, Fam107b and Tph2, showed differential expression in both transcriptomic and proteomic analysis. Forty-two overlapping proteins were identified compared with SCA patient serum, and Bayesian network analysis revealed that nilotinib treatment response was associated with the protein expression of CLU, CA2, GLUL, PRDX6, C1QA, PLXNB1, and age. These findings will serve as an important reference for future studies on the pathogenesis and discovery of druggable targets. </p>
Troriluzole in Adult Participants With Spinocerebellar Ataxia
ClinicalTrials.gov study NCT03701399. IPD Sharing: NO. Countries: 2. Publications: 3.
Trial in Adult Participants With Spinocerebellar Ataxia (SCA)
ClinicalTrials.gov study NCT02960893. IPD Sharing: NO. Countries: 1. Publications: 1.
Data from: Association of serum neurofilament light (sNfL) and disease severity in patients with spinocerebellar ataxia type 3
<p><a name="_Hlk22462511"><b>Objective:</b></a> To investigate serum neurofilament light protein (sNfL) levels in patients with spinocerebellar ataxia type 3 (SCA3) and to determine whether they are associated with disease severity.</p> <p><b>Methods: </b>This cross-sectional study enrolled 185 healthy controls and 235 <i>ATXN3</i> mutation carriers (17 asymptomatic stage, 20 preclinical stage, and 198 ataxic stage)<span class="fontstyle01"><span>. We measured </span></span>sNfL levels with the single molecule array (Simoa) platform. Clinical disease severity was assessed using the scale of assessment and rating of ataxia (SARA) and the inventory of non-ataxia signs (INAS). In a subgroup of 50 ataxic stage patients, we further evaluated the gray matter volume and the integrity of white matter fibers by magnetic resonance imaging (MRI).</p> <p><b>Results:</b> sNfL concentrations were elevated in asymptomatic, preclinical,<i> </i>and<i> </i>ataxic<i> ATXN3</i> mutation carriers compared to controls (12.18 [10.20-13.92], 21.84 [18.37-23.45], 36.06 [30.04-45.90] and 8.24 [5.92-10.84] pg/mL, median [interquartile range], respectively, <i>P </i>< 0·001). sNfL correlated with SARA (r=0.406, 95% confidence interval 0.284-0.515, <span class="fontstyle01"><span><i>P </i></span></span><span class="fontstyle01"><span>< 0.0001</span></span>) and INAS (r=0.375, 95% confidence interval 0.250-0.487, <span class="fontstyle01"><span><i>P </i></span></span><span class="fontstyle01"><span>< 0.0001</span></span>), and remained significant after adjustment for age and CAG repeats. In addition, we observed negative correlations of the sNfL with gray matter volume in the left precentral gyrus and the left paracentral lobule as well as with the mean diffusivity in widespread white matter tracts.</p> <p><b>Conclusion: </b>Our results demonstrate that sNfL levels are increased in <span class="fontstyle01"><span>SCA3</span></span> and are associated with clinical disease severity, which supports sNfL as a biomarker for disease severity in SCA3.</p>
On the redundancy of the Josephin domain (JD) containing proteins and implications on the spinocerebellar ataxia type 3 (SCA3)
<p>Docking of the PPI reported in Figure 2, 3A, 3B, 4, 5, and 6 of the manuscript ‘On the redundancy of the Josephin domain (JD) containing proteins and implications on the spinocerebellar ataxia type 3 (SCA3).’</p>
Lithium Treatment for Patients With Spinocerebellar Ataxia Type I
ClinicalTrials.gov study NCT00683943. IPD Sharing: Not stated. Countries: 1. Publications: 3.
Neuromuscular Electrical Stimulation on Median Nerve Facilitates Low Motor Cortex Excitability in Human With Spinocerebellar Ataxia
ClinicalTrials.gov study NCT02103075. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Priming Motor Learning Through Exercise in People With Spinocerebellar Ataxia
ClinicalTrials.gov study NCT05826171. IPD Sharing: NO. Countries: 1. Publications: 1.
Trans-spinal Electrical Stimulation in Individuals With Spinocerebellar Ataxia
ClinicalTrials.gov study NCT06267222. IPD Sharing: NO. Countries: 1. Publications: 19.
Cerebellar Transcranial Direct Current Stimulation in Spinocerebellar Ataxia 38
ClinicalTrials.gov study NCT05951010. IPD Sharing: NO. Countries: 1. Publications: 1.
Safety and Efficacy of Lithium Carbonate in Patients With Spinocerebellar Ataxia Type 3
ClinicalTrials.gov study NCT01096082. IPD Sharing: Not stated. Countries: 1. Publications: 3.
Measuring Neurological Impairment and Functional Visual Assessment In Spinocerebellar Ataxias
ClinicalTrials.gov study NCT00654251. IPD Sharing: Not stated. Countries: 1. Publications: 6.
Clinical Trial With Riluzole in Spinocerebellar Ataxia Type 2 (ATRIL)
ClinicalTrials.gov study NCT03347344. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Docosahexaenoic Acid (DHA) Replacement for Treatment in Spinocerebellar Ataxia 38
ClinicalTrials.gov study NCT03109626. IPD Sharing: YES. Countries: 1. Publications: 1.
Functional and Structural Imaging and Motor Control in Spinocerebellar Ataxia
ClinicalTrials.gov study NCT02488031. IPD Sharing: NO. Countries: 1. Publications: 12.
Data from: Association of serum neurofilament light (sNfL) and disease severity in patients with spinocerebellar ataxia type 3
Open the record for dataset details and reuse information.
Dalfampridine and Gait in Spinocerebellar Ataxias
ClinicalTrials.gov study NCT01811706. IPD Sharing: Not stated. Countries: 1. Publications: 0.
A Randomized, Parallel-arm, Double Blind, Placebo-controlled Study to Assess the Efficacy of Fampridine for Patients With Spinocerebellar Ataxia SCA27B Caused by a GAA Expansion in the FGF14 Gene
ClinicalTrials.gov study NCT07185347. IPD Sharing: YES. Countries: 1. Publications: 0.
Autosomal Dominant Spinocerebellar Ataxias and Social Cognition
ClinicalTrials.gov study NCT07099651. IPD Sharing: YES. Countries: 1. Publications: 0.
The Study of Transcranial Magnetic Stimulation in the Regulation of Spinocerebellar Ataxia
ClinicalTrials.gov study NCT06904716. IPD Sharing: YES. Countries: 1. Publications: 0.
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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.