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Hautakangas H, et al. Genome-wide analysis of 102,084 migraine cases. PMID 35115687

Design and scale

The meta-analysis included 102,084 cases and 771,257 controls. It identified 123 loci, 86 not previously reported. Subtype analysis included 29,679 cases with migraine subtype information.

Findings

  • Risk architecture implicated both neuronal and vascular genes/tissues.
  • Some loci were shared across migraine, while others showed stronger subtype associations.
  • The scale moved migraine genetics from rare familial channelopathies toward a highly polygenic common-disorder model.

Interpretation

The study supports mixed neuronal–vascular biology and provides target-discovery material. It does not create a clinical genetic diagnostic test: common variants have small effects, phenotype definitions vary and prediction portability depends on ancestry and ascertainment.

Limitations

  • European-ancestry dominance constrains global portability.
  • Case definitions and subtype assignment were heterogeneous.
  • Association does not identify the causal gene or therapeutic direction at each locus.
  • Aggregate risk prediction has not shown routine diagnostic or treatment-selection utility.

Knowledge-base use

Anchors biomarkers.md, trigeminovascular-biology-and-cgrp.md, and the overview’s statement that migraine is polygenic without a clinical genetic test.