Increased amyloid beta-peptide deposition in cerebral cortex as a consequence of apolipoprotein E genotype in late-onset Alzheimer disease - PubMed (original) (raw)

Increased amyloid beta-peptide deposition in cerebral cortex as a consequence of apolipoprotein E genotype in late-onset Alzheimer disease

D E Schmechel et al. Proc Natl Acad Sci U S A. 1993.

Abstract

Amyloid beta-peptide (A beta) deposition in senile plaques and cerebral vessels is a neuropathological feature of Alzheimer disease (AD). We examined the possibility that commonly observed variability in A beta deposition in late-onset AD might be related to apolipoprotein E genotype (APOE gene; the two most common alleles are 3 and 4), since APOE4 is a susceptibility gene for late-onset AD and apolipoprotein E interacts strongly with A beta in vitro. In an autopsy series of brains of late-onset AD patients, we found a strong association of APOE4 allele with increased vascular and plaque A beta deposits. Late-onset AD patients with one or two APOE4 alleles have a distinct neuropathological phenotype compared with patients homozygous for APOE3.

PubMed Disclaimer

Similar articles

Cited by

References

    1. Neurology. 1975 Feb;25(2):120-6 - PubMed
    1. Proc Natl Acad Sci U S A. 1993 Sep 1;90(17):8098-102 - PubMed
    1. Arch Neurol. 1985 Nov;42(11):1097-105 - PubMed
    1. Neurosci Lett. 1986 Jul 24;68(2):252-6 - PubMed
    1. Science. 1987 Feb 20;235(4791):873-7 - PubMed

Publication types

MeSH terms

Substances

LinkOut - more resources