ArticleCurrent genetic medicine reports2014
Genetic discoveries in AD using CSF amyloid and tau.
Article in Current genetic medicine reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed, 1 synthesis or guideline pooled it, 12 citations in OpenAlex.
- Genome-wide association study of CSF levels of 59 alzheimer's disease candidate proteins: significant associations with proteins involved in amyloid processing and inflammation.PLoS genetics · 2014Pooled it
- Alzheimer's disease-associated complement gene variants influence plasma complement protein levels.Journal of neuroinflammation · 2023Article
- Genetic architecture of plasma Alzheimer disease biomarkers.Human molecular genetics · 2023Article
- Genome-wide network-based pathway analysis of CSF t-tau/Aβ1-42 ratio in the ADNI cohort.BMC genomics · 2017Article
- Genetic Risk as a Marker of Amyloid-β and Tau Burden in Cerebrospinal Fluid.Journal of Alzheimer's disease : JAD · 2017Article
- Text mining facilitates database curation - extraction of mutation-disease associations from Bio-medical literature.BMC bioinformatics · 2015Article
- Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
The use of cerebrospinal fluid levels of Aβ42 and pTau181 as endophenotypes for genetic studies of Alzheimer's disease (AD) has led to successful identification of both rare and common AD risk variants. In addition, this approach has provided meaningful hypotheses for the biological mechanisms by which known AD risk variants modulate the disease process. In this article we discuss these successes and outline challenges to effective and continued applications of this approach. We contrast the statistical power of this approach with traditional case-control designs and discuss solutions to address challenges in quality control and data analysis for these phenotypes. Finally, we discuss the potential for the use of this approach with larger samples as well as the incorporation of next generation sequencing and for future work with other endophenotypes for AD.
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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.