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

Proc Natl Acad Sci U S A. 1993 Oct 15;90(20):9649-53. doi: 10.1073/pnas.90.20.9649.


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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Aged
  • Alzheimer Disease / genetics*
  • Alzheimer Disease / metabolism
  • Alzheimer Disease / pathology
  • Amyloid beta-Peptides / metabolism*
  • Apolipoproteins E / genetics*
  • Cerebral Amyloid Angiopathy / genetics
  • Cerebral Amyloid Angiopathy / pathology
  • Cerebral Cortex / metabolism*
  • Disease Susceptibility
  • Homozygote
  • Humans
  • Neurofibrillary Tangles / pathology
  • Neurofilament Proteins / metabolism
  • Prospective Studies
  • Retrospective Studies


  • Amyloid beta-Peptides
  • Apolipoproteins E
  • Neurofilament Proteins