Differential expression of gut miRNAs in idiopathic Parkinson's disease
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE145814 | GEO | 2021/07/14
REPOSITORIES: GEO
Similar Datasets
Project description:LRRK2 mutations are the most common genetic cause of Parkinson’s disease (PD). We performed a whole-genome RNA profiling of locus coeruleus post-mortem tissue from idiopathic PD (IPD) and LRRK2-associated PD patients. The differentially expressed genes found in IPD and LRRK2-associated PD were involved in the gene ontology terms of synaptic transmission and neuron projection. In addition, in the IPD group we found associated genes belonging to the immune system. Pathway analysis of the differentially expressed genes in IPD was related with neuroactive-ligand receptor interaction and with immune system pathways. Specifically, the analysis highlighted differential expression of genes located in the chromosome 6p21.3 belonging to the class II HLA. Our findings support the hypothesis of a potential role of neuroinflammation and the involvement of the HLA genetic area in IPD pathogenesis. Future studies are necessary to shed light on the relation of immune system related pathways in the etiopathogenesis of PD.
2012-06-01 | GSE34516 | GEO
Project description:LRRK2 mutations are the most common genetic cause of Parkinson’s disease (PD). We performed a whole-genome RNA profiling of putamen tissue from idiopathic PD (IPD), LRRK2-associated PD (G2019S mutation), neurologically healthy controls and one asymptomatic LRRK2 mutation carrier, by using the Genechip Human Exon 1.0-ST Array. The differentially expressed genes found in IPD revealed an alteration of biological pathways related to long term potentiation (LTP), GABA receptor signalling, and calcium signalling pathways, among others. These pathways are mainly related with cell signalling cascades and synaptic plasticity processes. They were also altered in the asymptomatic LRRK2 mutation carrier but not in the LRRK2-associated PD group. The expression changes seen in IPD might be attributed to an adaptive consequence of a dysfunction in the dopamine transmission. The lack of these altered molecular pathways in LRRK2-associated PD patients suggests that these cases could show a different molecular response to dopamine transmission impairment.
2011-11-10 | GSE23290 | GEO
Project description:Differential expression of gut miRNAs in idiopathic Parkinson's disease
| PRJNA608432 | ENA
Project description:Parkinson's disease (PD) is the second most common neurodegenerative disease after Alzheimer's disease. The purpose of this study was to analyze the profile of the tear proteome of patients with idiopathic PD (iPD), carriers of the E46K-SNCA mutation and healthy subjects (CT) and to identify biomarkers for the early diagnosis of PD. An observational, prospective and case-control pilot study was carried out in 24 patients with iPD, 3 carriers of the E46K-SNCA mutation and 27 CT subjects. The patients' neurological involvement was scored and their tear samples were analyzed using nano-liquid chromatography-mass spectrometry (nLC-MS/MS). These analyses led to the identification of 560 tear proteins in which some of the deregulated proteins were involved in immune response, apoptosis, collagen degradation, protein synthesis, defense and altered lysosomal function. Of these proteins, six related to neurodegenerative processes, showed a good capacity to classify patients and controls. These findings revealed that some proteins were upregulated in the tears of PD patients, mainly those involved in lysosomal function. It is worth highlighting the importance of this study in identifying tear proteins implicated in neurodegeneration and its relationship with PD patients with an aggressive disease phenotype.
2022-02-14 | PXD028811 | Pride
Project description:Idiopathic and LRRK2-associated Parkinson's disease
| PRJNA225813 | ENA
Project description:Neuroinflammation in the brain contributes to the pathogenesis of Parkinson’s disease (PD), but the potential dysregulation of peripheral immunity has not been systematically investigated for idiopathic PD (iPD). Here we showed an elevated peripheral cytotoxic immune milieu, with more terminally-differentiated effector memory (TEMRA) CD8 T, CD8+ NKT cells and circulating cytotoxic molecules in fresh blood of early-to-mid iPD, especially in females, after analyzing >700 innate and adaptive features. This profile, also reflected by fewer CD8+FOXP3+ regulatory T cells, was confirmed in another subcohort. Co-expression between cytotoxic molecules was selectively enhanced in CD8 TEMRA and effector memory (TEM) cells. Single-cell RNA-sequencing analysis demonstrated the accelerated CD8 differentiation within CD8 compartments, enhanced cytotoxic pathways in CD8 TEMRA and TEM cells, while CD8 central-memory (TCM) and naïve cells were already more-active and transcriptionally-reprogrammed. Our work provides a comprehensive map of dysregulated peripheral immunity in iPD, proposing previously-unrecognized candidates for early diagnosis and treatments.
2023-10-13 | GSE237254 | GEO
Project description:We performed Sequential Window Acquisition of all THeoretical Mass Spectra (SWATH-MS) on primary patient olfactory neuroepithelial derived cells (ONS) from both idiopathic PD (iPD) and healthy controls and identified 228 differentially quantified proteins. Reactome pathway analysis revealed that the “Neutrophil degranulation and XBP1(S) activates chaperone genes pathways” were the most affected, indicating disruption of the secretory pathway. Upon closer inspection we identified that proteins associated with the endoplasmic reticulum and the secretory pathways were the most abundantly changed, in particular proteins associated with the unfolded protein response (UPR). In order to validate this finding, we performed qRT-PCR analysis on patient ONS subjected to ER stressors and confirmed that the iPD patient cells had elevated UPR responses, in particular to tunicamycin mediated ER stress.
2022-05-20 | PXD030723 | Pride
Project description:Identification of early transcriptomic and metabolic alterations consistent across different idiopathic Parkinson’s disease (IPD) patients might reveal the potential basis of increased dopaminergic neuron vulnerability and primary disease mechanisms. In this study, we combine systems biology and data integration approaches to identify differences in transcriptomic and metabolic signatures between IPD patient and healthy individual-derived midbrain neural precursor cells. Characterization of gene expression and metabolic modeling reveal pyruvate, several amino acid and lipid metabolism as the most dysregulated metabolic pathways in IPD neural precursors. Furthermore, we show that IPD neural precursors endure mitochondrial metabolism impairment and a reduced total NAD pool. Accordingly, we show that treatment with NAD precursors increases ATP yield hence demonstrating a potential to rescue early IPD-associated metabolic changes.
2023-11-01 | GSE207088 | GEO
Project description:We analysed the RNA profile of IPSC-derived dopaminergic neurons from idiophatic and genetic form (LRRK2) of Parkinson’s disease (PD). Both, idiopathic and genetic form of the disease show similar expression alterations and were merged in one whole PD group. We found 437 differentially expressed genes (DEGs) in the PD group as a whole. Up-regulated DEGs (n=254) encompassed genes involved in neural functions and transcription factor functions whereas down-regulated DEGs (n=183) affected basic homeostasis. These data point towards the presence of gene - and also protein - expression changes in DAn from PD patients which co-occur simultaneously along with DNA methylation changes.
2015-12-01 | GSE51922 | GEO
Project description:The human olfactory epithelium represents a readily accessible source of adult neural cell types which can be propagated in vitro. We have used this feature to establish olfactory neurosphere-derived (hONS) cells lines from patients with idiopathic Parkinson's disease (PD) and healthy controls. We interrogated several metabolic activities of hONS cells from PD patients and detected significantly decreased levels of reduced glutathione and MTS [3- (4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium, inner salt] metabolism. Both were decreased to approximately 80% of control donor hONS cell levels. These decreases did not correlate with any other known parameter, such as donor age or gender nor with the number of passages in vitro. Therefore we conclude that the differences are either symptomatic of PD or reflect an underlying predisposition for PD. Transcriptomic analysis identified the xenobiotic and anti-oxidant pathways, mediated by the aryl hydrocarbon receptor and NRF2, respectively, as significantly dysregulated in PD hONS cells. We show here that activation of the NRF2 pathway, by ectopic L-sulforaphane treatment, increased total glutathione and MTS metabolism levels to control-donor hONS cell levels in 12 of 14 hONS cell lines established from 14 individual donors with idiopathic PD. The importance of our results is three-fold. Firstly, they corroborated data obtained from in vivo and other in vitro cell models but uniquely on varied human genetic backgrounds. Secondly, they demonstrate that cells from PD patients are responsive to NRF2 pathway activation. Finally, they suggest that the dysregulation of the NRF2 pathway is not merely symptomatic of PD but may be a contributing factor.
2011-07-14 | E-TABM-879 | biostudies-arrayexpress