ArticleJournal of Alzheimer's disease : JAD2014
Genetic interactions within inositol-related pathways are associated with longitudinal changes in ventricle size.
Article in Journal of Alzheimer's disease : JAD, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 21 citations in OpenAlex.
- DJ-1-mediated repression of the RNA-binding protein FMRP is predicted to impact known Alzheimer's disease-related protein networks.Journal of Alzheimer's disease : JAD · 2024Article
- Transcriptomic Analysis of Lipid Metabolism Genes in Alzheimer's Disease: Highlighting Pathological Outcomes and Compartmentalized Immune Status.Journal of molecular neuroscience : MN · 2024Article
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- HENA, heterogeneous network-based data set for Alzheimer's disease.Scientific data · 2019Article
- An in-silico approach for discovery of microRNA-TF regulation of DISC1 interactome mediating neuronal migration.NPJ systems biology and applications · 2019Article
- Sequence analysis and structure prediction of ABHD16A and the roles of the ABHD family members in human disease.Open biology · 2018Review
- Genetics of Alzheimer's Disease: the Importance of Polygenic and Epistatic Components.Current neurology and neuroscience reports · 2017Review
- Recent publications from the Alzheimer's Disease Neuroimaging Initiative: Reviewing progress toward improved AD clinical trials.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2017Review
- Exploring the interaction among EPHX1, GSTP1, SERPINE2, and TGFB1 contributing to the quantitative traits of chronic obstructive pulmonary disease in Chinese Han population.Human genomics · 2016Article
- Discovery of gene-gene interactions across multiple independent data sets of late onset Alzheimer disease from the Alzheimer Disease Genetics Consortium.Neurobiology of aging · 2016Article
- Identification of putative SNPs in progressive retinal atrophy affected Canis lupus familiaris using exome sequencing.Mammalian genome : official journal of the International Mammalian Genome Society · 2015Article
- Trans effects of chromosome aneuploidies on DNA methylation patterns in human Down syndrome and mouse models.Genome biology · 2015Article
- Genetic studies of quantitative MCI and AD phenotypes in ADNI: Progress, opportunities, and plans.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2015Review
- Genetic modification of the relationship between phosphorylated tau and neurodegeneration.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2014Article
- Chronic periodontitis genome-wide association studies: gene-centric and gene set enrichment analyses.Journal of dental research · 2014Article
- Genetic variation modifies risk for neurodegeneration based on biomarker status.Frontiers in aging neuroscience · 2014Article
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4 authors at 1 institution in 1 country.
Funding
Abstract
The genetic etiology of late-onset Alzheimer's disease (LOAD) has proven complex, involving clinical and genetic heterogeneity and gene-gene interactions. Recent genome wide association studies in LOAD have led to the discovery of novel genetic risk factors; however, the investigation of gene-gene interactions has been limited. Conventional genetic studies often use binary disease status as the primary phenotype, but for complex brain-based diseases, neuroimaging data can serve as quantitative endophenotypes that correlate with disease status and closely reflect pathological changes. In the Alzheimer's Disease Neuroimaging Initiative cohort, we tested for association of genetic interactions with longitudinal MRI measurements of the inferior lateral ventricles (ILVs), which have repeatedly shown a relationship to LOAD status and progression. We performed linear regression to evaluate the ability of pathway-derived SNP-SNP pairs to predict the slope of change in volume of the ILVs. After Bonferroni correction, we identified four significant interactions in the right ILV (RILV) corresponding to gene-gene pairs SYNJ2-PI4KA, PARD3-MYH2, PDE3A-ABHD12B, and OR2L13-PRKG1 and one significant interaction in the left ILV (LILV) corresponding to SYNJ2-PI4KA. The SNP-SNP interaction corresponding to SYNJ2-PI4KA was identical in the RILV and LILV and was the most significant interaction in each (RILV: p = 9.13 × 10(-12); LILV: p = 8.17 × 10(-13)). Both genes belong to the inositol phosphate signaling pathway which has been previously associated with neurodegeneration in AD and we discuss the possibility that perturbation of this pathway results in a down-regulation of the Akt cell survival pathway and, thereby, decreased neuronal survival, as reflected by increased volume of the ventricles.
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