Evidence map›Paper›PMID 40725463›Full record

ArticleGenes2025

Gene-Based Burden Testing of Rare Variants in Hemiplegic Migraine: A Computational Approach to Uncover the Genetic Architecture of a Rare Brain Disorder.

Mohammed M Alfayyadh, Neven Maksemous, Heidi G Sutherland, Rodney A Lea, Lyn R Griffiths

Abstract read
In one paragraph

Article in Genes, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Hemiplegic migraine: genetics and pathophysiology.The Journal of clinical investigation · 2026
    Review
  2. 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

5 authors.

Mohammed M AlfayyadhCentre for Genomics and Personalised Health, Genomics Research Centre, School of Biomedical Sciences, Queensland University of Technology (QUT), Brisbane, QLD 4059, Australia.ORCID 0000-0003-1481-6046
Neven MaksemousCentre for Genomics and Personalised Health, Genomics Research Centre, School of Biomedical Sciences, Queensland University of Technology (QUT), Brisbane, QLD 4059, Australia.ORCID 0000-0002-4891-4333
Heidi G SutherlandCentre for Genomics and Personalised Health, Genomics Research Centre, School of Biomedical Sciences, Queensland University of Technology (QUT), Brisbane, QLD 4059, Australia.ORCID 0000-0002-8512-1498
Rodney A LeaCentre for Genomics and Personalised Health, Genomics Research Centre, School of Biomedical Sciences, Queensland University of Technology (QUT), Brisbane, QLD 4059, Australia.
Lyn R GriffithsCentre for Genomics and Personalised Health, Genomics Research Centre, School of Biomedical Sciences, Queensland University of Technology (QUT), Brisbane, QLD 4059, Australia.ORCID 0000-0002-6774-5475

Funding

Australian Government EIF Super Science Funds Queensland Node project (LRG)Australian International Science Linkages grant LRGAustralian National Health and Medical Research Council APP1122387Migraine Research Foundation grant (2016), NY, USA (2016), NY, USA (LRG)
6 · The paper itself

Abstract

backgroundHM is a rare, severe form of migraine with aura, characterised by motor weakness and strongly influenced by genetic factors affecting the brain. While pathogenic variants in

methodsTo advance our understanding of HM, we applied a variant prioritisation approach using whole-exome sequencing (WES) data from patients referred for HM diagnosis (n = 184) and utilised PathVar, a bioinformatics pipeline designed to identify pathogenic variants. Our analysis incorporated two strategies for association testing: (1) PathVar-identified single nucleotide variants (SNVs) and (2) PathVar SNVs combined with missense and rare variants. Principal component analysis (PCA) was performed to adjust for ancestral and other unknown differences between cases and controls.

resultsOur results reveal a sequential reduction in the number of genes significantly associated with HM, from 20 in the first strategy to 11 in the second, which highlights the unique contribution of PathVar SNVs to the genetic architecture of HM. PathVar SNVs were more distinctive in the case cohort, suggesting a closer link to the functional changes underlying HM compared to controls. Notably, novel genes, such as

conclusionsBy prioritising PathVar SNVs, we identified a broader set of genes potentially contributing to HM. Given that HM is a rare condition, our findings, utilising a sample size of 184, represent a unique contribution to the field. This iterative analysis demonstrates that integrating diverse variant schemes provides a more comprehensive view of the genetic factors driving HM.

Indexed as

Migraine with AuraAdultCalcium ChannelsCalcium Channels, N-TypeComputational BiologyExome SequencingFemaleGenetic Predisposition to DiseaseHumansMaleMiddle AgedNAV1.1 Voltage-Gated Sodium ChannelPolymorphism, Single NucleotideSodium-Potassium-Exchanging ATPaseATP1A2 protein, humanCACNA1A protein, humanCalcium ChannelsCalcium Channels, N-TypeNAV1.1 Voltage-Gated Sodium ChannelSCN1A protein, humanSodium-Potassium-Exchanging ATPaseassociation analysisbioinformaticsburden testinghemiplegic migrainePathVar

Identifiers

PMID40725463
PMCPMC12294318

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Registered trials

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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.