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Gene expression data from induced Pluripotent Stem cells from Parkinson's Disease patients harbouring amplification of, or mutations in the SNCA gene, and from healthy control donors

ABSTRACT: Gene expression data from induced Pluripotent Stem cells from Parkinson's Disease patients harbouring amplification of, or mutations in the SNCA gene, and from healthy control donors

PROVIDER: PRJNA353643 | ENA |

REPOSITORIES: ENA

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Gene expression data from induced Pluripotent Stem cells from Parkinson's Disease patients harbouring amplification of, or mutations in the SNCA gene, and from healthy control donors

Project description:This SuperSeries is composed of the SubSeries listed below.

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Gene expression data from induced Pluripotent Stem cells from Parkinson's Disease patients harbouring amplification of, or mutations in the SNCA gene, and from healthy control donors [genotype]

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Gene expression data from induced Pluripotent Stem cells from Parkinson's Disease patients harbouring amplification of, or mutations in the SNCA gene, and from healthy control donors [gene expression]

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Brain transcriptomic analysis in Parkinson's disease patients stratified by Braak Lewy body stage / Sex differences in Parkinson's disease brain transcriptome

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Project description:Genome-wide association studies (GWAS) have uncovered thousands of single nucleotide polymorphisms (SNPs) that are associated with Parkinson's disease (PD) risk. The functions of most of these SNPs, including the cell type they influence, and how they affect PD etiology remain largely unknown. To identify functional SNPs, we aligned PD risk SNPs within active regulatory regions of DNA in microglia, a cell type implicated in PD development. Out of 6,749 ‘SNPs of interest’ from the most recent PD GWAS metanalysis, 73 were located in open regulatory chromatin as determined by both ATAC-seq and H3K27ac ChIP-seq. We identified an active enhancer in microglia in intron two of SNCA that overlaps two PD risk SNPs, rs2737004 and rs2619356. In iPSC-derived microglia, CRISPR/Cas9 deletion of the open chromatin encompassing these SNPs caused reduced expression of multiple genes including SNCA and the adjacent gene MMRN1. Loss of the enhancer also led to upregulation of genes involved in glucose metabolism, a process that is known to be altered in PD patients. Our work expands the role of SNCA in Parkinson’s Disease and provides a connection between PD-associated genetic variants and underlying biology that points to a risk mechanism in microglia.

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Parkinson's Disease Risk Enhancers in Microglia [ATAC-seq]

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Transcriptome datasets of neural progenitors and neurons differentiated from induced pluripotent stem cells of healthy donors and Parkinson's disease patients with mutations in PARK2 gene

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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.

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