Evidence map›Paper›PMID 28987266›Full record

ReviewTrends in genetics : TIG2017

The Genetics of Multiple Sclerosis: From 0 to 200 in 50 Years.

Sergio E Baranzini, Jorge R Oksenberg

Abstract readReview
In one paragraph

Review in Trends in genetics : TIG, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 109 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
109citing papers in PubMed, 3 pooled it
18.9field-weighted citation impact, top 1% 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

109 citing papers in PubMed, 3 syntheses or guidelines pooled it, 243 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. The genetic effect of theBioscience reports · 2018
    Pooled it
  4. Article
  5. Article
  6. Review
  7. Integrated multi-omics and machine learning prioritize key immune genes for multiple sclerosis risk prediction.Mammalian genome : official journal of the International Mammalian Genome Society · 2026
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Divergent T Cell Phenotypes Define Pediatric Crohn's Disease and Ulcerative Colitis.medRxiv : the preprint server for health sciences · 2025
    Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article

49 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Sergio E BaranziniWeill Institute for Neurosciences. Department of Neurology, University of California San Francisco, San Francisco, CA, USA; Institute for Human Genetics, University of California San Francisco, San Francisco, CA, USA; Graduate Program in Bioinformatics, University of California San Francisco, San Francisco, CA, USA. Electronic address: Sergio.baranzini@ucsf.edu.
Jorge R OksenbergWeill Institute for Neurosciences. Department of Neurology, University of California San Francisco, San Francisco, CA, USA; Institute for Human Genetics, University of California San Francisco, San Francisco, CA, USA.
University of California, San Francisco · US

Funding

GENE LINKAGE STUDY OF MULTIPLE SCLEROSIS SIBLING PAIRSR01NS026799 · NINDS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI HAUSER, STEPHEN L, OKSENBERG, JORGE R. · 1989 to 2018
$6.8M
Post GWAS approach to identify cell-specific genetic pathways underlying MS riskR01NS088155 · NINDS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI BARANZINI, SERGIO E · 2014 to 2018
$2.2M
NINDS NIH HHS R01 NS026799NINDS NIH HHS R01 NS088155
6 · The paper itself

Abstract

Multiple sclerosis (MS) is a common autoimmune disease that targets myelin in the central nervous system (CNS). Multiple genome-wide association studies (GWAS) over the past 10 years have uncovered more than 200 loci that independently contribute to disease pathogenesis. As with many other complex diseases, risk of developing MS is driven by multiple common variants whose biological effects are not immediately clear. Here, we present a historical perspective on the progress made in MS genetics and discuss current work geared towards creating a more complete model that accurately represents the genetic landscape of MS susceptibility. Such a model necessarily includes a better understanding of the individual contributions of each common variant to the cellular phenotypes, and interactions with other genes and with the environment. Future genetic studies in MS will likely focus on the role of rare variants and endophenotypes.

Indexed as

Genetic Predisposition to DiseaseGenetic VariationGenome-Wide Association StudyHumansMultiple SclerosisPhenotypegene regulatory networksgenetic pathwaysGWASmultiple sclerosis

Identifiers

PMID28987266
PMCPMC5701819
OpenAlexW2763147694

What OpenQuestion holds

Textmetadata
LicenceTDM
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.