SynthesisHuman genetics2006
Towards compendia of negative genetic association studies: an example for Alzheimer disease.
Synthesis in Human genetics, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 7 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
16 citing papers in PubMed, 7 syntheses or guidelines pooled it.
- Angiotensin-converting enzyme polymorphisms AND Alzheimer's disease susceptibility: An updated meta-analysis.PloS one · 2021Pooled it
- Nitride oxide synthase 3 and klotho gene polymorphisms in the pathogenesis of chronic kidney disease and age-related cognitive impairment: a systematic review and meta-analysis.F1000Research · 2020Pooled it
- Polymorphisms of CHAT but not TFAM or VR22 are Associated with Alzheimer Disease Risk.Medical science monitor : international medical journal of experimental and clinical research · 2016Pooled it
- The nitric oxide synthase 3 G894T polymorphism associated with Alzheimer's disease risk: a meta-analysis.Scientific reports · 2015Pooled it
- Lack of association between cathepsin D C224T polymorphism and Alzheimer's disease risk: an update meta-analysis.BMC neurology · 2014Pooled it
- Meta-analysis of the association between urokinase-plasminogen activator gene rs2227564 polymorphism and Alzheimer's disease.American journal of Alzheimer's disease and other dementias · 2013Pooled it
- Interleukin-1A -889C/T polymorphism and risk of Alzheimer's disease: a meta-analysis based on 32 case-control studies.Journal of neurology · 2012Pooled it
- Genetic Factors Affecting Late-Onset Alzheimer's Disease Susceptibility.Neuromolecular medicine · 2016Article
- Study of Alzheimer family case reveals hemochromotosis-associated HFE mutation.Human genome variation · 2014Article
- Genetic association of urokinase-type plasminogen activator gene rs2227564 site polymorphism with sporadic Alzheimer's disease in the Han Chinese population.Neural regeneration research · 2012Article
- Association of the RAGE G82S polymorphism with Alzheimer's disease.Journal of neural transmission (Vienna, Austria : 1996) · 2010Article
- Whole genome association analysis shows that ACE is a risk factor for Alzheimer's disease and fails to replicate most candidates from Meta-analysis.International journal of molecular epidemiology and genetics · 2010Article
- HGVbaseG2P: a central genetic association database.Nucleic acids research · 2009Article
- Tau as a biomarker of neurodegenerative diseases.Biomarkers in medicine · 2008Article
- Genetics of Alzheimer's disease: a centennial review.Neurologic clinics · 2007Review
- Association study on chromosome 20q11.21-13.13 locus and its contribution to type 2 diabetes susceptibility in Japanese.Human genetics · 2006Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Most genetic sequence variants that contribute to variability in complex human traits will have small effects that are not readily detectable with population samples typically used in genetic association studies. A potentially valuable tool in the gene discovery process is meta-analysis of the accumulated published data, but in order to be valid these require a sample of studies representative of the true genetic effect and thus hypothetically should include some positive and an abundance of negative reports. A survey of the literature on association studies for Alzheimer disease (AD) from January 2004-April 2005, identified 138 studies, 86 of which reported positive findings other than for apolipoprotein E (APOE), strongly indicative of publication bias. We report here an analysis of 62 genetic markers, tested for association with AD risk as well as for possible effects upon quantitative indices of AD severity (mini-mental state examination scores, age-at-onset, and cerebrospinal fluid (CSF) beta-amyloid (Abeta) and CSF tau proteins). Within this set, only modest signals were present that, with the exception of APOE are easily lost when corrections for multiple hypotheses are applied. In isolation, results are thus broadly negative. Genes studied encompass both novel candidates as well as several recently claimed to be associated with AD (e.g. urokinase plasminogen activator (PLAU) and acetyl-coenzyme A acetyltransferase 1 (ACAT1)). By reporting these data we hope to encourage the publication of gene compendia to guide further studies and aid future meta-analyses aimed at resolving the involvement of genes in complex human traits.
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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.