Evidence map›Paper›PMID 24794218›Full record

ArticlePloS one2014

The refinement of genetic predictors of multiple sclerosis.

Giulio Disanto, Ruth Dobson, Julia Pakpoor, Ramyiadarsini I Elangovan, Rocco Adiutori, Jens Kuhle, Gavin Giovannoni

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.9field-weighted citation impact, top 16% 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

8 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Gene-Environment Interactions in Multiple Sclerosis: A UK Biobank Study.Neurology(R) neuroimmunology & neuroinflammation · 2021
    Article
  5. Review
  6. Review
  7. Article
  8. Burden of genetic risk variants in multiple sclerosis families in the Netherlands.Multiple sclerosis journal - experimental, translational and clinical
    Article
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

7 authors at 3 institutions in 1 country.

Giulio DisantoQueen Mary University of London, Blizard Institute, Barts and The London School of Medicine and Dentistry, London, United Kingdom.
Ruth DobsonQueen Mary University of London, Blizard Institute, Barts and The London School of Medicine and Dentistry, London, United Kingdom.
Julia PakpoorOxford medical school, University of Oxford, John Radcliffe Hospital, Oxford, United Kingdom.
Ramyiadarsini I ElangovanOxford medical school, University of Oxford, John Radcliffe Hospital, Oxford, United Kingdom.
Rocco AdiutoriQueen Mary University of London, Blizard Institute, Barts and The London School of Medicine and Dentistry, London, United Kingdom.
Jens KuhleQueen Mary University of London, Blizard Institute, Barts and The London School of Medicine and Dentistry, London, United Kingdom.
Gavin GiovannoniQueen Mary University of London, Blizard Institute, Barts and The London School of Medicine and Dentistry, London, United Kingdom.
Queen Mary University of London · GBJohn Radcliffe Hospital · GBUniversity of Oxford · GB

Funding

Medical Research Council G0801976
6 · The paper itself

Abstract

A recent genome wide association study (GWAS) demonstrated that more than 100 genetic variants influence the risk of multiple sclerosis (MS). We investigated what proportion of the general population can be considered at high genetic risk of MS, whether genetic information can be used to predict disease development and how the recently found genetic associations have influenced these estimates. We used summary statistics from GWAS in MS to estimate the distribution of risk within a large simulated general population. We profiled MS associated loci in 70 MS patients and 79 healthy controls (HC) and assessed their position within the distribution of risk in the simulated population. The predictive performance of a weighted genetic risk score (wGRS) on disease status was investigated using receiver operating characteristic statistics. When all known variants were considered, 40.8% of the general population was predicted to be at reduced risk, 49% at average, 6.9% at elevated and 3.3% at high risk of MS. Fifty percent of MS patients were at either reduced or average risk of disease. However, they showed a significantly higher wGRS than HC (median 13.47 vs 12.46, p = 4.08×10(-10)). The predictive performance of the model including all currently known MS associations (area under the curve = 79.7%, 95%CI = 72.4%-87.0%) was higher than that of models considering previously known associations. Despite this, considering the relatively low prevalence of MS, the positive predictive value was below 1%. The increasing number of known associated genetic variants is improving our ability to predict the development of MS. This is still unlikely to be clinically useful but a more complete understanding of the complexity underlying MS aetiology and the inclusion of environmental risk factors will aid future attempts of disease prediction.

Indexed as

Genetic VariationComputer SimulationGenetic Predisposition to DiseaseGenome-Wide Association StudyHumansModels, GeneticModels, StatisticalMultiple SclerosisRisk Factors

Identifiers

PMID24794218
PMCPMC4008598
OpenAlexW2003416002

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.