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  • Rivier, Cyprien A (author)

Polygenic Risk of Epilepsy and Post-Stroke Epilepsy.

  • Article/chapterEnglish2023

Publisher, publication year, extent ...

  • 2023

Numbers

  • LIBRIS-ID:oai:gup.ub.gu.se/330866
  • https://gup.ub.gu.se/publication/330866URI
  • https://doi.org/10.1101/2023.09.18.23295739DOI

Supplementary language notes

  • Language:English

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  • Subject category:ref swepub-contenttype
  • Subject category:art swepub-publicationtype

Notes

  • Epilepsy is highly heritable, with numerous known genetic risk loci. However, the genetic predisposition's role in post-acute brain injury epilepsy remains understudied. This study assesses whether a higher genetic predisposition to epilepsy raises post-stroke or Transient Ischemic Attack (TIA) survivor's risk of Post-Stroke Epilepsy (PSE).We conducted a three-stage genetic analysis. First, we identified independent epilepsy-associated ( p <5x10 -8 ) genetic variants from public data. Second, we estimated PSE-specific variant weights in stroke/TIA survivors from the UK Biobank. Third, we tested for an association between a polygenic risk score (PRS) and PSE risk in stroke/TIA survivors from the All of Us Research Program. Primary analysis included all ancestries, while a secondary analysis was restricted to European ancestry only. A sensitivity analysis excluded TIA survivors. Association testing was conducted via multivariable logistic regression, adjusting for age, sex, and genetic ancestry.Among 19,708 UK Biobank participants with stroke/TIA, 805 (4.1%) developed PSE. Likewise, among 12,251 All of Us participants with stroke/TIA, 394 (3.2%) developed PSE. After establishing PSE-specific weights for 39 epilepsy-linked genetic variants in the UK Biobank, the resultant PRS was associated with elevated odds of PSE development in All of Us (OR:1.16[1.02-1.32]). A similar result was obtained when restricting to participants of European ancestry (OR:1.23[1.02-1.49]) and when excluding participants with a TIA history (OR:1.18[1.02-1.38]).Our findings suggest that akin to other forms of epilepsy, genetic predisposition plays an essential role in PSE. Because the PSE data were sparse, our results should be interpreted cautiously.

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Added entries (persons, corporate bodies, meetings, titles ...)

  • Clocchiatti-Tuozzo, Santiago (author)
  • Misra, Shubham (author)
  • Zelano, Johan,1981Gothenburg University,Göteborgs universitet,Extern,Wallenberg Centre for Molecular and Translational Medicine,Institutionen för neurovetenskap och fysiologi, sektionen för klinisk neurovetenskap,External,Institute of Neuroscience and Physiology, Department of Clinical Neuroscience(Swepub:gu)xzeljo (author)
  • Mazumder, Rajarshi (author)
  • Sansing, Lauren H (author)
  • de Havenon, Adam (author)
  • Hirsch, Lawrence J (author)
  • Liebeskind, David S (author)
  • Gilmore, Emily J (author)
  • Sheth, Kevin N (author)
  • Kim, Jennifer A (author)
  • Worrall, Bradford B (author)
  • Falcone, Guido (author)
  • Mishra, Nishant K (author)
  • Göteborgs universitetExtern (creator_code:org_t)

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  • In:medRxiv : the preprint server for health sciences

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