SynthesisMolecular biology reports2013
Pathway analysis of genome-wide association studies for Parkinson's disease.
Synthesis in Molecular biology reports, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
12 citing papers in PubMed, 24 citations in OpenAlex.
- Somatic Mutations Detected in Parkinson Disease Could Affect Genes With a Role in Synaptic and Neuronal Processes.Frontiers in aging · 2022Article
- Cholecystectomy and subsequent risk of Parkinson's disease: a nationwide retrospective cohort study.NPJ Parkinson's disease · 2021Article
- Molecular and Functional Analysis of Sunitinib-Resistance Induction in Human Renal Cell Carcinoma Cells.International journal of molecular sciences · 2021Article
- Article
- The association betweenBrain and behavior · 2018Article
- Parallel roles of transcription factors dFOXO and FER2 in the development and maintenance of dopaminergic neurons.PLoS genetics · 2018Article
- From Genomics to Omics Landscapes of Parkinson's Disease: Revealing the Molecular Mechanisms.Omics : a journal of integrative biology · 2018Article
- A Review of Pathway-Based Analysis Tools That Visualize Genetic Variants.Frontiers in genetics · 2017Review
- Bile Acids in Neurodegenerative Disorders.Frontiers in aging neuroscience · 2016Review
- Pathway analysis of two amyotrophic lateral sclerosis GWAS highlights shared genetic signals with Alzheimer's disease and Parkinson's disease.Molecular neurobiology · 2015Article
- Genome-wide association studies in neurology.Annals of translational medicine · 2014Review
- A conserved role for p48 homologs in protecting dopaminergic neurons from oxidative stress.PLoS genetics · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The study was done to identify the candidate causal single nucleotide polymorphisms (SNPs) and candidate causal mechanisms that contribute to Parkinson's disease (PD) susceptibility and to generate a SNP to ene to pathway hypothesis using an analytical pathway-based approach. We used a PD genome-wide association study (GWAS) meta-analysis data of the genotypes of 2,525,705 SNPs in 4,238 PD cases and 4,239 controls. Identify candidate Causal SNPs and Pathways (ICSNPathway) analysis was applied to the PD GWAS dataset. The first stage involved the pre-selection of candidate causal SNPs by linkage disequilibrium analysis and the functional SNP annotation of the most significant SNPs found. The second stage involved the annotation of biological mechanisms for the pre-selected candidate causal SNPs using improved-gene set enrichment analysis. ICSNPathway analysis identified three candidate SNPs, two genes, twenty-one pathways, and three hypothetical biological mechanisms: (1) rs17651549 to microtubule-associated protein tau (MAPT) to protein domain specific binding (nominal p < 0.001, false discovery rate (FDR) < 0.001), neurogenesis (nominal p < 0.001, FDR < 0.001), regulation of neurogenesis (nominal p < 0.001, FDR = 0.001), positive regulation of axonogenesis (nominal p < 0.001, FDR = 0.001), regulation of protein polymerization (nominal p < 0.001, FDR = 0.004), negative regulation of organelle organization (nominal p < 0.001, FDR = 0.004), hsa01510 (nominal p < 0.001, FDR = 0.005), neuron differentiation (nominal p < 0.001, FDR = 0.009), and axonogenesis (nominal p < 0.001, FDR = 0.009); (2) rs10445337 to MAPT to protein domain specific binding (nominal p < 0.001, FDR < 0.001), neurogenesis (nominal p < 0.001, FDR < 0.001), regulation of neurogenesis (nominal p < 0.001, FDR = 0.001), and positive regulation of axonogenesis (nominal p < 0.001, FDR = 0.001); (3) rs9938550 to HSD3B7 to hsa00363 (nominal p < 0.001, FDR = 0.004), bile acid metabolic process (nominal p = 0.005, FDR = 0.019), and steroid metabolic process (nominal p = 0.010, FDR = 0.039). By applying the ICSNPathway analysis to PD GWAS meta-analysis data, three candidate SNPs, two genes (MAPT and HSD3B7), and 21 pathways involving protein domain specific binding and neurogenesis were identified, which may contribute to PD susceptibility.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.