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

D. E. Schmechel, A. M. Saunders, W. J. Strittmatter, B. J. Crain, C. M. Hulette, S. H. Joo, M. A. Pericak-Vance, D. Goldgaber, A. D. Roses

Research output: Contribution to journalArticlepeer-review

Abstract

Amyloid β-peptide (Aβ) deposition in senile plaques and cerebral vessels is a neuropathological feature of Alzheimer disease (AD). We examined the possibility that commonly observed variability in Aβ 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 Aβ 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 Aβ deposits. Late-onset AD patients with one or two APOE4 alleles have a distinct neuropathological phenotype compared with patients homozygous for APOE3.

Original languageEnglish (US)
Pages (from-to)9649-9653
Number of pages5
JournalProceedings of the National Academy of Sciences of the United States of America
Volume90
Issue number20
DOIs
StatePublished - Oct 15 1993

Keywords

  • APOE4 gene
  • Phenotype

ASJC Scopus subject areas

  • General

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