Evidence map›Paper›PMID 22072275›Full record

ReviewThe journal of headache and pain2012

Genetics of migraine in the age of genome-wide association studies.

Markus Schürks

Open access · goldAbstract readReview
In one paragraph

Review in The journal of headache and pain, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
6.7field-weighted citation impact, top 2% 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

38 citing papers in PubMed, 96 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Genetic Mechanisms of Migraine: Insights from Monogenic Migraine Mutations.International journal of molecular sciences · 2023
    Review
  5. Article
  6. Review
  7. Genetic Variation inJournal of cardiovascular development and disease · 2022
    Article
  8. Article
  9. Article
  10. Review
  11. Observational
  12. Article
  13. Article
  14. Association of MTHFR gene polymorphisms with migraine in North Indian population.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2018
    Article
  15. Article
  16. Involvement of the Tetraspanin 2 (Frontiers in neurology · 2018
    Article
  17. Article
  18. Review
  19. Article
  20. Association ofIranian journal of public health · 2016
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

Markus SchürksDepartment of Neurology, University Hospital Essen, Hufelandstrasse 55, 45122, Essen, Germany. markus.schuerks@uni-due.de
Essen University Hospital · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Genetic factors importantly contribute to migraine. However, unlike for rare monogenic forms of migraine, approaches to identify genes for common forms of migraine have been of limited success. Candidate gene association studies were often negative and positive results were often not replicated or replication failed. Further, the significance of positive results from linkage studies remains unclear owing to the inability to pinpoint the genes under the peaks that may be involved in migraine. Problems hampering these studies include limited sample sizes, methods of migraine ascertainment, and the heterogeneous clinical phenotype. Three genome-wide association studies are available now and have successfully identified four new genetic variants associated with migraine. One new variant (rs1835740) modulates glutamate homeostasis, thus integrates well with current concepts of neurotransmitter disturbances. This variant may be more specific for severe forms of migraine such as migraine with aura than migraine without aura. Another variant (rs11172113) implicates the lipoprotein receptor LRP1, which may interact with neuronal glutamate receptors, thus also providing a link to the glutamate pathway. In contrast, rs10166942 is in close proximity to TRPM8, which codes for a cold and pain sensor. For the first time this links a gene explicitly implicated in pain related pathways to migraine. The potential function of the fourth variant rs2651899 (PRDM16) in migraine is unclear. All these variants only confer a small to moderate change in risk for migraine, which concurs with migraine being a heterogeneous disorder. Ongoing large international collaborations will likely identify additional gene variants for migraine.

Indexed as

Genetic Predisposition to DiseaseGenome-Wide Association StudyDNA-Binding ProteinsHumansLow Density Lipoprotein Receptor-Related Protein-1Migraine DisordersPolymorphism, Single NucleotideTranscription FactorsTRPM Cation ChannelsDNA-Binding ProteinsLow Density Lipoprotein Receptor-Related Protein-1LRP1 protein, humanPRDM16 protein, humanTranscription FactorsTRPM8 protein, humanTRPM Cation Channels

Identifiers

PMID22072275
PMCPMC3253157
OpenAlexW2028643581

What OpenQuestion holds

Textmetadata
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.