Methylation profiling by array for Parkinson's disease using brain tissue
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PROVIDER: PRJNA802252 | ENA |
REPOSITORIES: ENA
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Project description:Parkinson’s disease is second most prevalent neurodegenerative disorder. Parkinson’s disease is hypothesized to be caused by a multifaceted interplay between genetic and environmental factors. We profiled the DNA methylation using the frontal lobe from people who died from Parkinson’s disease and compared them with age-, and sex-matched controls. We hypothesized that the complex regulation of DNA methylation and metabolome leads to deficits that cause irregular motor function among Parkinson’s disease subjects and the metabolomic disparities may reflect the effect of these complex interactions. Herein, we aim to integrate quantitative metabolomics and DNA methylation of brain tissue from primary motor cortex (Brodmann area 4) from Parkinson’s disease sufferers to better understand the biochemistry associated with the onset of the disease. Parkinson’s disease (PD) is second most prevalent neurodegenerative disorder following Alzheimer’s disease. Parkinson’s disease is hypothesized to be caused by a multifaceted interplay between genetic and environmental factors. Herein, and for the first time, we describe the integration of metabolomics and epigenetics (genome-wide DNA methylation; epimetabolomics) to profile the frontal lobe from people who died from PD and compared them with age-, and sex-matched controls. We identified 48 metabolites to be at significantly different concentrations (FDR q<0.05), 4,313 differentially methylated sites [5'-C-phosphate-G-3' (CpGs)] (FDR q<0.05) and increased DNA methylation age in the primary motor cortex of people who died from PD. We identified Primary bile acid biosynthesis as the major biochemical pathway to be perturbed in the frontal lobe of PD sufferers, and the metabolite taurine (p-value = 5.91E-06) as being positively correlated with CpG cg14286187 (SLC25A27; CYP39A1) (FDR q = 0.002), highlighting previously unreported biochemical changes associated with PD pathogenesis. In this novel multi-omics study, we identify regulatory mechanisms which we believe warrant future translational investigation and central biomarkers of PD which require further validation in more accessible biomatrices.
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Project description:Transcriptional analysis of multiple brain regions in Parkinson's disease supports the involvement of specific protein processing, energy metabolism, and signaling pathways, and suggests novel disease mechanisms. This SuperSeries is composed of the SubSeries listed below.
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Project description:To investigate transcriptomic changes associated with Parkinson's disease development we compared frontal cortex gene expression across four Braak Lewy body stage groups. Additionally we investigated sex-specific gene expression differences in neuropathologically healthy donors and Parkinson's disease patients at Braak Lewy body stage 5. We investigated sex-specific gene expression differences in neuropathologically healthy donors and Parkinson's disease patients at Braak Lewy body stage 5.
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Project description:Genome-wide transcriptome analysis of expression changes in laser-dissected SNpc neurons from Parkinson's disease brain tissue versus control brain tissue. Post-mortem brain expression analysis performed in 10 PD brain samples and 8 control brain samples.
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Project description:Genome-wide transcriptome analysis of expression changes in Globus Pallidus interna (GPi) from Parkinson's disease brain tissue versus control brain tissue. Post-mortem brain expression analysis performed in 10 PD brain samples and 10 control brain samples.
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Project description:Detailed analysis of disease-affected tissue provides insight into molecular mechanisms contributing to pathogenesis. Substantia nigra, striatum and cortex are functionally connected with increasing degrees of alpha-synuclein pathology in Parkinson's disease. Functional and causal pathway analysis of gene expression and proteomic alterations in these three regions revealed pathways that correlated with deposition of alpha-synuclein. Microarray and RNAseq experiments revealed previously unidentified causal changes related to oligodendrocyte function and synaptic vesicle release and other changes were reflected across all brain regions. Importantly a subset of these changes were replicated in Parkinson's disease blood. Proteomic assessment revealed alterations in mitochondria and vesicular transport proteins that preceded gene gene expression changes indicating defects in translation and/or protein turnover. Our combined approach of proteomics, RNAseq and microarray analyses provides a comprehensive view of the molecular changes that accompany alpha-synculein pathology in Parkinson's disease, and may be instrumental in understanding and diagnosing Parkinson's disease progression. Substantia Nigra (3 normal, 3 PD), Striatum (6 normal, 6 PD), Cortex (5 normal, 5 PD), Cortex non-PD neurodegeneration (2 normal, 3 DLB). Note Sample X201264 was used both for Cortex normal and for Cortex nonPD normal
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