No association between the intronic Presenilin-1 polymorphism and Alzheimer's disease in clinic and population-based samples

Xingang Cai, Judith Stanton, Dani Fallin, Jonathan Hoyne, Ranjan Duara, Michael Gold, Steve Sevush, Paul Scibelli, Fiona Crawford, Michael Mullan

Research output: Contribution to journalArticle

23 Scopus citations

Abstract

Mutations in the Presenilin 1 (PS1) gene on chromosome 14 cause most early-onset familial Alzheimer's disease (AD). An intronic polymorphism in the PS1 gene was recently identified and reported to be associated with late-onset AD [Wragg et al., Lancet 347: 509-512, 1996]. The authors found an excess of homozygotes for the more common allele (allele 1) in AD cases, associated with an approximate doubling of risk. In the present study, we report the PSI polymorphism distributions in clinic and population-based samples. We were not able to replicate the findings of Wragg et al. [1996]. Our results are consistent with those of other researchers and do not support the conclusion that the PS1 polymorphism is associated with late- onset AD.

Original languageEnglish (US)
Pages (from-to)202-203
Number of pages2
JournalAmerican Journal of Medical Genetics - Neuropsychiatric Genetics
Volume74
Issue number2
DOIs
StatePublished - 1997

Keywords

  • Alzheimer's disease
  • polymorphism
  • psi gene

ASJC Scopus subject areas

  • Genetics(clinical)
  • Neuropsychology and Physiological Psychology
  • Neuroscience(all)

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