ArticleTrends in genetics : TIG2010
Towards a complete resolution of the genetic architecture of disease.
Article in Trends in genetics : TIG, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 3 of them syntheses 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
46 citing papers in PubMed, 3 syntheses or guidelines pooled it, 88 citations in OpenAlex.
- TREM2 variants in Alzheimer's disease.The New England journal of medicine · 2013Pooled it
- Using genome-wide complex trait analysis to quantify 'missing heritability' in Parkinson's disease.Human molecular genetics · 2012Pooled it
- Imputation of sequence variants for identification of genetic risks for Parkinson's disease: a meta-analysis of genome-wide association studies.Lancet (London, England) · 2011Pooled it
- Integrated Assays of Genome-Wide Association Study, Multi-Omics Co-Localization, and Machine Learning Associated Calcium Signaling Genes with Oilseed Rape Resistance toInternational journal of molecular sciences · 2024Article
- Cohort Profile: The Alliance for Maternal and Newborn Health Improvement (AMANHI) biobanking study.International journal of epidemiology · 2022Article
- The Road so Far in Colorectal Cancer Pharmacogenomics: Are We Closer to Individualised Treatment?Journal of personalized medicine · 2020Review
- QTG-Finder: A Machine-Learning Based Algorithm To Prioritize Causal Genes of Quantitative Trait Loci in Arabidopsis and Rice.G3 (Bethesda, Md.) · 2019Article
- Article
- Genetic and epigenetic influences on the loss of tolerance in autoimmunity.Cellular & molecular immunology · 2018Review
- Analysis of the prion protein gene in multiple system atrophy.Neurobiology of aging · 2017Article
- Multiple system atrophy: genetic risks and alpha-synuclein mutations.F1000Research · 2017Review
- Severe axonal neuropathy is a late manifestation of SPG11.Journal of neurology · 2016Article
- Evaluation of DNMT1 gene expression profile and methylation of its promoter region in patients with ankylosing spondylitis.Clinical rheumatology · 2016Article
- Next-generation sequencing in neuromuscular diseases.Current opinion in neurology · 2016Review
- Genome-wide assessment of Parkinson's disease in a Southern Spanish population.Neurobiology of aging · 2016Article
- Clinical Trial Simulations Based on Genetic Stratification and the Natural History of a Functional Outcome Measure in Creutzfeldt-Jakob Disease.JAMA neurology · 2016Article
- Epigenetics of multiple sclerosis: an updated review.Neuromolecular medicine · 2015Review
- Genetic causes of amyotrophic lateral sclerosis: new genetic analysis methodologies entailing new opportunities and challenges.Brain research · 2015Review
- Next generation sequencing techniques in neurological diseases: redefining clinical and molecular associations.Human molecular genetics · 2014Review
- Association of μ-opioid receptor gene (OPRM1) haplotypes with postoperative nausea and vomiting.Experimental brain research · 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
4 authors at 3 institutions in 2 countries.
Funding
Abstract
After years of linear gains in the genetic dissection of human disease we are now in a period of exponential discovery. This is particularly apparent for complex disease. Genome-wide association studies (GWAS) have provided myriad associations between common variability and disease, and have shown that common genetic variability is unlikely to explain the entire genetic predisposition to disease. Here we detail how one can expand on this success and systematically identify genetic risks that lead or predispose to disease using next-generation sequencing. Geneticists have had for many years a protocol to identify Mendelian disease. A similar set of tools is now available for the identification of rare moderate-risk loci and common low-risk variants. Whereas major challenges undoubtedly remain, particularly regarding data handling and the functional classification of variants, we suggest that these will be largely practical and not conceptual.
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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.