ArticleNature2013
Integrative genomics identifies APOE ε4 effectors in Alzheimer's disease.
Article in Nature, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 84 papers, 4 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
84 citing papers in PubMed, 4 syntheses or guidelines pooled it, 147 citations in OpenAlex.
- Meta-Analysis of Differential Connectivity in Gene Co-Expression Networks in Multiple Sclerosis.International journal of molecular sciences · 2016Pooled it
- Thyrotropin and Alzheimer's Disease Risk in the Elderly: a Systematic Review and Meta-Analysis.Molecular neurobiology · 2016Pooled it
- Integrated genomic approaches identify major pathways and upstream regulators in late onset Alzheimer's disease.Scientific reports · 2015Pooled it
- Apolipoprotein E gene polymorphism and Alzheimer's disease in Chinese population: a meta-analysis.Scientific reports · 2014Pooled it
- Trial
- Response of the medial temporal lobe network in amnestic mild cognitive impairment to therapeutic intervention assessed by fMRI and memory task performance.NeuroImage. Clinical · 2015Trial
- Predicting the apolipoprotein E ε4 allele carrier status based on gray matter volumes and cognitive function.Brain and behavior · 2024Article
- Bayesian Machine Learning Enables Identification of Transcriptional Network Disruptions Associated with Drug-Resistant Prostate Cancer.Cancer research · 2023Article
- Quercetin Is An Active Agent in Berries against Neurodegenerative Diseases Progression through Modulation of Nrf2/HO1.Nutrients · 2022Review
- Predictability of polygenic risk score for progression to dementia and its interaction with APOE ε4 in mild cognitive impairment.Translational neurodegeneration · 2021Article
- Review
- Postseptic Cognitive Impairment and Expression of APOE in Peripheral Blood: The Cognition After SepsiS (CASS) Observational Pilot Study.Journal of intensive care medicine · 2021Observational
- The Synaptic Vesicle Protein 2A Interacts With Key Pathogenic Factors in Alzheimer's Disease: Implications for Treatment.Frontiers in cell and developmental biology · 2021Article
- Amyloidogenic processing of amyloid β protein precursor (APP) is enhanced in the brains of alcadein α-deficient mice.The Journal of biological chemistry · 2020Article
- A review of the current concerns about misconduct in medical sciences publications and the consequences.Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2020Review
- Gain and loss events in the evolution of the apolipoprotein family in vertebrata.BMC evolutionary biology · 2019Article
- Article
- A small molecule ApoE4-targeted therapeutic candidate that normalizes sirtuin 1 levels and improves cognition in an Alzheimer's disease mouse model.Scientific reports · 2018Article
- Systematic Analysis and Biomarker Study for Alzheimer's Disease.Scientific reports · 2018Article
- Evolutionary footprint of epistasis.PLoS computational biology · 2018Article
24 more citing papers are in PubMed but not listed here.
Corrections and comments
- Retraction · 2015-07-17Error in Image · Falsification/Fabrication of Image · Manipulation of Images · Unreliable Image ·
- Commented on by
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- Retracted
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Late-onset Alzheimer's disease (LOAD) risk is strongly influenced by genetic factors such as the presence of the apolipoprotein E ε4 allele (referred to here as APOE4), as well as non-genetic determinants including ageing. To pursue mechanisms by which these affect human brain physiology and modify LOAD risk, we initially analysed whole-transcriptome cerebral cortex gene expression data in unaffected APOE4 carriers and LOAD patients. APOE4 carrier status was associated with a consistent transcriptomic shift that broadly resembled the LOAD profile. Differential co-expression correlation network analysis of the APOE4 and LOAD transcriptomic changes identified a set of candidate core regulatory mediators. Several of these--including APBA2, FYN, RNF219 and SV2A--encode known or novel modulators of LOAD associated amyloid beta A4 precursor protein (APP) endocytosis and metabolism. Furthermore, a genetic variant within RNF219 was found to affect amyloid deposition in human brain and LOAD age-of-onset. These data implicate an APOE4 associated molecular pathway that promotes LOAD.
Indexed as
Identifiers
What OpenQuestion holds
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.