NINDS Parkinson’s Disease
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA330889 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:NINDS Inherited Forms of Motor Neuron Disease Study
| PRJNA377929 | ENA
Project description:Advanced age represents one of the major risk factors for Parkinson’s Disease. Recent studies posit a role for microRNAs in Parkinson’s Disease and it is well established that microRNAs are remodelled during ageing, but the relationship between the two processes have not been clarified yet. The aim of the present study is to unravel the relevance of microRNAs as biomarkers of Parkinson’s Disease within the ageing framework. We used Next Generation Sequencing to profile serum microRNAs from samples informative for Parkinson’s Disease (recently diagnosed, drug-naïve Parkinson’s Disease patients) and healthy ageing (centenarians) plus healthy controls age-matched with Parkinson’s Disease patients. Potential candidates, emerging from the combination of differential expression and network analyses, were further validated in an independent cohort including both drug-naïve and advanced Parkinson’s Disease patients together with healthy siblings of Parkinson’s Disease patients at higher genetic risk for Parkinson’s Disease. While we did not find evidences of microRNAs co-regulated in Parkinson’s Disease and ageing, we report that hsa-miR-144-3p is consistently down-regulated in early and advanced Parkinson’s Disease and in Parkinson’s Disease siblings. Interestingly, functional analysis revealed that hsa-miR-144-3p is involved in the regulation of coagulation, a process known to be altered in Parkinson’s Disease. Our results consistently show the down-regulation of hsa-mir144-3p in early and advanced Parkinson’s Disease, robustly confirmed across a variety of analytical and experimental analyses. These results are promising, and additional research is needed to unveil the functional details of its relevance and involvement in Parkinson’s Disease.
2022-02-02 | GSE180193 | GEO
Project description:Mitochondrial DNA allelic substitutions in Parkinson’s disease
| PRJNA453701 | ENA
Project description:In these studies, we used splice variant-specific microarrays manufactured by the ExonHit company ( www.exonhit.com) on the Affymetrix platform. The goal was to identify splice isoforms whose expression is altered in whole blood of early-stage Parkinson’s disease patients compared to healthy and neurodegenerative disease controls. The study included 19 cases of Parkinson’s disease (PD) samples, 4 of multiple system atrophy (MSA), 4 progressive supranuclear palsy (PSP) and 10 healthy controls. Thirteen splice variants were confirmed in quantitative polymerase chain reactions and used to classify blinded samples from Parkinson’s disease patients and controls with 90% accuracy and 94% sensitivity.
2012-12-01 | GSE34287 | GEO
Project description:Proteomic and targeted metabolomic studies on a silkworm model of Parkinson’s disease
2022-03-14 | PXD032252 |
Project description:Mitochondrial DNA (mtDNA) damage is considered as a possible primary cause of Parkinson’s disease (PD). To explore the issue, mtDNA sequences from whole blood were analyzed in PD patients and controls using a resequencing chip and allelic substitutions were estimated for each nucleotide position (np) along the entire mtDNA sequence. Overall, 58 np showed a different allelic distribution in the two groups; of these, 81% showed an increase of non-reference alleles in PD patients, similar to findings reported in patients with Alzheimer’s disease, albeit in reduced proportion. These results suggest that age-related neurodegenerative diseases could share a mechanism involving mtDNA.
2019-05-21 | GSE113704 | GEO
Project description:Improved diagnostic and prognostic biomarkers which reflect pathological progression would benefit the management of Parkinson’s disease. GPR37, also known as parkin associated endothelin-like (Pael) receptor, is an orphan G protein-coupled receptor, which has a defective parkin-mediated ubiquitination in autosomal recessive Parkinson’s disease. By means of immunoblot and mRNA determinations we detected increased GPR37 levels in postmortem substantia nigra from Parkinson’s disease subjects. We revealed the presence of the N-terminal domain of GPR37 (ecto-GPR37) in human and mouse cerebrospinal fluid (CSF). We engineered a Nanoluciferase-based ELISA to evaluate ecto-GPR37 in CSF and demonstrated the presence of ecto-GPR37 in CSF from wild-type, but not from GPR37-/-, mice. Subsequently, the relative abundance of ecto-GPR37 in CSF in healthy controls (n=48) and Parkinson’s disease (n=45) patients was assessed. Interestingly, we found that ecto-GPR37 was significantly increased (P = 0.0002) in the CSF from Parkinson’s disease patients. Importantly, mass spectrometric analysis of immunoprecipitation of GPR37 in CSF supported the analytical validity of our ELISA to measure ecto-GPR37 in human CSF. Overall, these results open exciting perspectives and encourage further systemically studies to confirm the clinical validity and utility of ecto-GPR37 as a potential Parkinson’s disease diagnostic/prognostic biomarker
2021-05-13 | PXD015619 | Pride
Project description:In this exploratory study, we used laser microdissection to extract dopaminergic neurons from 10 human SNpc samples obtained at autopsy in Parkinson’s disease patients and control subjects. Extracted RNA and proteins were identified by RNA sequencing and nano-LC-MS/MS, respectively, and the differential expression between Parkinson’s disease and control group was assessed.
2021-06-30 | GSE169755 | GEO
Project description:We have used microarrays to analyze gene expression in Parkinson’s disease (PD). We used four different brain regions, including two that are relatively affected in PD (striatum and cortex) and two that are relatively spared (cerebellum and medulla). We show that while differences between brain regions are strong, expression profile differences between PD and controls are much more modest and that genome-wide significant differences are restricted to the striatum and cerebral cortex. RNA (aRNA) was generated from 500ng of total RNA from the medulla (n=15 control brains, n=14 PD brains), striatum (n=15 control brains, n = 15 PD brains), frontal cortex (n=15 control brains, n = 11 PD brains) and cerebellum (n = 14 control brains, n=15 PD brains).
2011-07-21 | E-GEOD-28894 | biostudies-arrayexpress