Article
A FE65 polymorphism associated with risk of developing sporadic late-onset alzheimer's disease but not with Abeta loading in brains.
Neuroscience letters - 20 Oct 2000
Lambert J C, Mann D, Goumidi L, Harris J, Pasquier F, Frigard B, Cottel D, Lendon C, Iwatsubo T, Amouyel P, Chartier-Harlin M C
Abstract excerpt
The FE65 protein was previously described interacting with amyloid protein precursor (APP) and mediating its internalization. Hu et al. (Hum. Genet., 103 (1998) 295) recently reported that a deletion polymorphism in intron 13 of the FE65 gene may be protective for sporadic Alzheimer's disease (AD) forms and suggested that this deletion may modify splicing between exon 13 and 14 (the two exons encoding the...
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