Failure to detect missense mutations in the S182 gene in a series of late-onset Alzheimer's disease cases.
The possibility of an interaction of multiple genes has been speculated in pathogenesis of Alzheimer's disease (AD). Because we have recently cloned a novel gene S182 bearing five different missense mutations which segregate with early-onset familial AD, we sought the frequency of these mutations in familial and sporadic late-onset AD to clarify the incidence of these mutations in the disease. The current study showed lack of these mutations in 118 independent subjects affected with late-onset Alzheimer's disease.
Tsuda
T
T
Department of Medicine, Centre for Research in Neurodegenerative Diseases, University of Toronto, Canada.
Chi
H
H
Liang
Y
Y
Rogaeva
E A
EA
Sherrington
R
R
Levesque
G
G
Ikeda
M
M
Rogaev
E I
EI
Pollen
D
D
Freedman
M
M
D000368:Aged; D000544:Alzheimer Disease / Q000235:genetics*; D001483:Base Sequence; D003001:Cloning, Molecular; D017931:DNA Primers; D005796:Genes; D006801:Humans; D008565:Membrane Proteins / Q000235:genetics*; D008969:Molecular Sequence Data; D009154:Mutation / Q000235:genetics* / Q000502:physiology; D016133:Polymerase Chain Reaction; D053764:Presenilin-1
D017931:DNA Primers; D008565:Membrane Proteins; C508853:PSEN1 protein, human; D053764:Presenilin-1