Evidence map›Paper›PMID 29740026›Full record

SynthesisScientific reports2018

Lack of genetic support for shared aetiology of Coronary Artery Disease and Late-onset Alzheimer's disease.

Christopher Grace, Robert Clarke, Anuj Goel, Martin Farrall, Hugh Watkins, Jemma C Hopewell

Open access · goldAbstract readMeta-Analysis
PubMed Full text at PMC Publisher
In one paragraph

Synthesis in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 1 pooled it
0.9field-weighted citation impact, top 22% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

14 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Alterations in the inflammatory homeostasis of aging-related cardiac dysfunction and Alzheimer's diseases.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Christopher GraceDivision of Cardiovascular Medicine, Radcliffe Department of Medicine, University of Oxford, Oxford, UK. cgrace@well.ox.ac.uk.
Robert ClarkeClinical Trial Service Unit and Epidemiological Studies Unit, Nuffield Department of Population Health, University of Oxford, Oxford, UK.
Anuj GoelDivision of Cardiovascular Medicine, Radcliffe Department of Medicine, University of Oxford, Oxford, UK.ORCID 0000-0003-2307-4021
Martin FarrallDivision of Cardiovascular Medicine, Radcliffe Department of Medicine, University of Oxford, Oxford, UK.
Hugh WatkinsDivision of Cardiovascular Medicine, Radcliffe Department of Medicine, University of Oxford, Oxford, UK.
Jemma C HopewellClinical Trial Service Unit and Epidemiological Studies Unit, Nuffield Department of Population Health, University of Oxford, Oxford, UK.
Centre for Human Genetics · GBUniversity of Oxford · GB

Funding

British Heart Foundation CH/1996001/9454British Heart Foundation FS/14/55/30806British Heart Foundation RE/13/1/30181Medical Research CouncilWellcome TrustWellcome Trust 090532/Z/09/Z
6 · The paper itself

Abstract

Epidemiological studies suggest a positive association between coronary artery disease (CAD) and late-onset Alzheimer's disease (LOAD). This large-scale genetic study brings together 'big data' resources to examine the causal impact of genetic determinants of CAD on risk of LOAD. A two-sample Mendelian randomization approach was adopted to estimate the causal effect of CAD on risk of LOAD using summary data from 60,801 CAD cases from CARDIoGRAMplusC4D and 17,008 LOAD cases from the IGAP Consortium. Additional analyses assessed the independent relevance of genetic associations at the APOE locus for both CAD and LOAD. Higher genetically determined risk of CAD was associated with a slightly higher risk of LOAD (Odds Ratio (OR) per log-odds unit of CAD [95% CI]: 1.07 [1.01-1.15]; p = 0.027). However, after exclusion of the APOE locus, the estimate of the causal effect of CAD for LOAD was attenuated and no longer significant (OR 0.94 [0.88-1.01]; p = 0.072). This Mendelian randomization study indicates that the APOE locus is the chief determinant of shared genetic architecture between CAD and LOAD, and suggests a lack of causal relevance of CAD for risk of LOAD after exclusion of APOE.

Indexed as

Genetic Predisposition to DiseaseMendelian Randomization AnalysisAgedAlzheimer DiseaseCoronary Artery DiseaseFemaleGenome-Wide Association StudyHumansMaleMiddle AgedPhenotypePolymorphism, Single NucleotideRisk AssessmentRisk Factors

Identifiers

PMID29740026
PMCPMC5940751
OpenAlexW2800487862

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.