No genetic association between Fyn kinase gene polymorphisms (-93A/G, IVS10+37T/C and Ex12+894T/G) and Japanese sporadic Alzheimer's disease

Neurosci Lett. 2004 Apr 22;360(1-2):109-11. doi: 10.1016/j.neulet.2004.02.046.

Abstract

Several groups have reported that abnormal phosphorylation of tau by Fyn, a protein-tyrosine kinase, may play a role in the neuropathogenesis of Alzheimer's disease (AD). In the present study, three common Japanese polymorphisms of the Fyn gene (-93A/G in the 5'-flanking region, IVS10+37T/C in intron 10 and Ex12+894T/G in the 3'-untranslated region) were studied in 127 healthy controls and 182 sporadic AD cases using a polymerase chain reaction restriction fragment length polymorphism method. A comparison of the allelic and genotypic frequencies of these polymorphisms between controls and sporadic AD cases failed to show any significant difference. These results suggest that the Fyn polymorphisms (-93A/G, IVS10+37T/C and Ex12+894T/G) investigated here have no genetic association with sporadic AD.

Publication types

  • Comparative Study

MeSH terms

  • Adult
  • Aged
  • Aged, 80 and over
  • Alzheimer Disease / enzymology
  • Alzheimer Disease / genetics*
  • Chi-Square Distribution
  • Female
  • Gene Frequency / genetics
  • Genetic Linkage / genetics*
  • Humans
  • Japan
  • Male
  • Middle Aged
  • Polymorphism, Genetic / genetics*
  • Proto-Oncogene Proteins / genetics*
  • Proto-Oncogene Proteins c-fyn

Substances

  • Proto-Oncogene Proteins
  • FYN protein, human
  • Proto-Oncogene Proteins c-fyn