Rare Functional Variant in TM2D3 is Associated with Late-Onset Alzheimer's Disease

نویسندگان

  • Johanna Jakobsdottir
  • Sven J van der Lee
  • Joshua C Bis
  • Vincent Chouraki
  • David Li-Kroeger
  • Shinya Yamamoto
  • Megan L Grove
  • Adam Naj
  • Maria Vronskaya
  • Jose L Salazar
  • Anita L DeStefano
  • Jennifer A Brody
  • Albert V Smith
  • Najaf Amin
  • Rebecca Sims
  • Carla A Ibrahim-Verbaas
  • Seung-Hoan Choi
  • Claudia L Satizabal
  • Oscar L Lopez
  • Alexa Beiser
  • M Arfan Ikram
  • Melissa E Garcia
  • Caroline Hayward
  • Tibor V Varga
  • Samuli Ripatti
  • Paul W Franks
  • Göran Hallmans
  • Olov Rolandsson
  • Jan-Håkon Jansson
  • David J Porteous
  • Veikko Salomaa
  • Gudny Eiriksdottir
  • Kenneth M Rice
  • Hugo J Bellen
  • Daniel Levy
  • Andre G Uitterlinden
  • Valur Emilsson
  • Jerome I Rotter
  • Thor Aspelund
  • Christopher J O'Donnell
  • Annette L Fitzpatrick
  • Lenore J Launer
  • Albert Hofman
  • Li-San Wang
  • Julie Williams
  • Gerard D Schellenberg
  • Eric Boerwinkle
  • Bruce M Psaty
  • Sudha Seshadri
  • Joshua M Shulman
  • Vilmundur Gudnason
  • Cornelia M van Duijn
چکیده

We performed an exome-wide association analysis in 1393 late-onset Alzheimer's disease (LOAD) cases and 8141 controls from the CHARGE consortium. We found that a rare variant (P155L) in TM2D3 was enriched in Icelanders (~0.5% versus <0.05% in other European populations). In 433 LOAD cases and 3903 controls from the Icelandic AGES sub-study, P155L was associated with increased risk and earlier onset of LOAD [odds ratio (95% CI) = 7.5 (3.5-15.9), p = 6.6x10-9]. Mutation in the Drosophila TM2D3 homolog, almondex, causes a phenotype similar to loss of Notch/Presenilin signaling. Human TM2D3 is capable of rescuing these phenotypes, but this activity is abolished by P155L, establishing it as a functionally damaging allele. Our results establish a rare TM2D3 variant in association with LOAD susceptibility, and together with prior work suggests possible links to the β-amyloid cascade.

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عنوان ژورنال:

دوره 12  شماره 

صفحات  -

تاریخ انتشار 2016