SynthesisHuman genetics2011
Investigation of 15 of the top candidate genes for late-onset Alzheimer's disease.
Synthesis in Human genetics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
27 citing papers in PubMed, 1 synthesis or guideline pooled it, 57 citations in OpenAlex.
- Long Non-coding RNA: Insight Into Mechanisms of Alzheimer's Disease.Frontiers in molecular neuroscience · 2021Pooled it
- Novel Alzheimer's disease genes and epistasis identified using machine learning GWAS platform.Scientific reports · 2023Article
- Polymorphism rs11867353 of Tyrosine Kinase Non-Receptor 1 (TNK1) Gene Is a Novel Genetic Marker for Alzheimer's Disease.Molecular neurobiology · 2021Article
- Review
- HippocampalInternational journal of molecular sciences · 2019Article
- A Generic Sure Independence Screening Procedure.Journal of the American Statistical Association · 2019Article
- Alzheimer's Disease Risk Variant rs2373115 Regulates GAB2 and NARS2 Expression in Human Brain Tissues.Journal of molecular neuroscience : MN · 2018Article
- Spontaneous development of Alzheimer's disease-associated brain pathology in a Shugoshin-1 mouse cohesinopathy model.Aging cell · 2018Article
- The impact ofAnnals of translational medicine · 2018Article
- De Novo Mutations in EBF3 Cause a Neurodevelopmental Syndrome.American journal of human genetics · 2017Article
- Alzheimer's Disease: Biomarkers in the Genome, Blood, and Cerebrospinal Fluid.Frontiers in neurology · 2017Review
- 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
- Genetic Interactions Explain Variance in Cingulate Amyloid Burden: An AV-45 PET Genome-Wide Association and Interaction Study in the ADNI Cohort.BioMed research international · 2015Article
- Genetic, transcriptomic, and epigenetic studies of HIV-associated neurocognitive disorder.Journal of acquired immune deficiency syndromes (1999) · 2014Review
- Genetic interactions associated with 12-month atrophy in hippocampus and entorhinal cortex in Alzheimer's Disease Neuroimaging Initiative.Neurobiology of aging · 2013Article
- Regulation of distinct pools of amyloid β-protein by multiple cellular proteases.Alzheimer's research & therapy · 2013Review
- Linking protective GAB2 variants, increased cortical GAB2 expression and decreased Alzheimer's disease pathology.PloS one · 2013Article
- Alzheimer's disease risk alleles in TREM2 illuminate innate immunity in Alzheimer's disease.Alzheimer's research & therapy · 2013Review
- Replication of association between schizophrenia and chromosome 6p21-6p22.1 polymorphisms in Chinese Han population.PloS one · 2013Article
- An integrative network algorithm identifies age-associated differential methylation interactome hotspots targeting stem-cell differentiation pathways.Scientific reports · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 5 institutions in 3 countries.
Funding
Abstract
The 12 genome-wide association studies (GWAS) published to-date for late-onset Alzheimer's disease (LOAD) have identified over 40 candidate LOAD risk modifiers, in addition to apolipoprotein (APOE) ε4. A few of these novel LOAD candidate genes, namely BIN1, CLU, CR1, EXOC3L2 and PICALM, have shown consistent replication, and are thus credible LOAD susceptibility genes. To evaluate other promising LOAD candidate genes, we have added data from our large, case-control series (n=5,043) to meta-analyses of all published follow-up case-control association studies for six LOAD candidate genes that have shown significant association across multiple studies (TNK1, GAB2, LOC651924, GWA_14q32.13, PGBD1 and GALP) and for an additional nine previously suggested candidate genes. Meta-analyses remained significant at three loci after addition of our data: GAB2 (OR=0.78, p=0.007), LOC651924 (OR=0.91, p=0.01) and TNK1 (OR=0.92, p=0.02). Breslow-Day tests revealed significant heterogeneity between studies for GAB2 (p<0.0001) and GWA_14q32.13 (p=0.006). We have also provided suggestive evidence that PGBD1 (p=0.04) and EBF3 (p=0.03) are associated with age-at-onset of LOAD. Finally, we tested for interactions between these 15 genes, APOE ε4 and the five novel LOAD genes BIN1, CLU, CR1, EXOC3L2 and PICALM but none were significant after correction for multiple testing. Overall, this large, independent follow-up study for 15 of the top LOAD candidate genes provides support for GAB2 and LOC651924 (6q24.1) as risk modifiers of LOAD and novel associations between PGBD1 and EBF3 with age-at-onset.
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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.