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Analysis of the KIFAP3 gene in amyotrophic lateral sclerosis: A multicenter survival study

  • Perry T.C. van Doormaal
  • , Nicola Ticozzi
  • , Cinzia Gellera
  • , Antonia Ratti
  • , Franco Taroni
  • , Adriano Chiò
  • , Andrea Calvo
  • , Gabriele Mora
  • , Gabriella Restagno
  • , Bryan J. Traynor
  • , Anna Birve
  • , Robin Lemmens
  • , Michael A. van Es
  • , Christiaan G.J. Saris
  • , Hylke M. Blauw
  • , Paul W.J. van Vught
  • , Ewout J.N. Groen
  • , Lucia Corrado
  • , Letizia Mazzini
  • , Roberto Del Bo
  • Stefania Corti, Stefan Waibel, Thomas Meyer, Albert C. Ludolph, An Goris, Philip van Damme, Wim Robberecht, Aleksey Shatunov, Isabella Fogh, Peter M. Andersen, Sandra D'Alfonso, Orla Hardiman, Simon Cronin, Dan Rujescu, Ammar Al-Chalabi, John E. Landers, Vincenzo Silani, Leonard H. van den Berg, Jan H. Veldink

Research output: Contribution to journalArticlepeer-review

Abstract

Sporadic amyotrophic lateral sclerosis is a multifactorial disease of environmental and genetic origin. In a previous large multicenter genome wide study, common genetic variation in the Kinesin-Associated Protein 3 (KIFAP3) gene (rs1541160) was reported to have a significant effect on survival in amyotrophic lateral sclerosis patients. However, this could not be replicated in 3 smaller independent cohorts. We conducted a large multicenter multivariate survival analysis (n= 2362) on the effect of genetic variation in rs1541160. The previously reported beneficial genotype did not show a significant improvement in survival in this patient group.

Original languageEnglish
Pages (from-to)2420.e13-2420.e14
JournalNeurobiology of Aging
Volume35
Issue number10
DOIs
Publication statusPublished - Oct 2014

Keywords

  • Amyotrophic lateral sclerosis
  • Genome-wide association study
  • KIFAP3
  • Kinesin-associated protein 3 gene

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