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 journalArticle

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
StatePublished - Oct 15 1993
Externally publishedYes

Fingerprint

Apolipoproteins E
Amyloid
Cerebral Cortex
Alzheimer Disease
Genotype
Peptides
Alleles
Amyloid Plaques
Genes
Blood Vessels
Autopsy
Phenotype
Brain

Keywords

  • APOE4 gene
  • Phenotype

ASJC Scopus subject areas

  • General
  • Genetics

Cite this

Schmechel, D. E., Saunders, A. M., Strittmatter, W. J., Crain, B. J., Hulette, C. M., Joo, S. H., ... Roses, A. D. (1993). Increased amyloid β-peptide deposition in cerebral cortex as a consequence of apolipoprotein E genotype in late-onset Alzheimer disease. Proceedings of the National Academy of Sciences of the United States of America, 90(20), 9649-9653.

Increased amyloid β-peptide deposition in cerebral cortex as a consequence of apolipoprotein E genotype in late-onset Alzheimer disease. / Schmechel, D. E.; Saunders, A. M.; Strittmatter, W. J.; Crain, B. J.; Hulette, C. M.; Joo, S. H.; Pericak-Vance, M. A.; Goldgaber, D.; Roses, A. D.

In: Proceedings of the National Academy of Sciences of the United States of America, Vol. 90, No. 20, 15.10.1993, p. 9649-9653.

Research output: Contribution to journalArticle

Schmechel, DE, Saunders, AM, Strittmatter, WJ, Crain, BJ, Hulette, CM, Joo, SH, Pericak-Vance, MA, Goldgaber, D & Roses, AD 1993, 'Increased amyloid β-peptide deposition in cerebral cortex as a consequence of apolipoprotein E genotype in late-onset Alzheimer disease', Proceedings of the National Academy of Sciences of the United States of America, vol. 90, no. 20, pp. 9649-9653.
Schmechel, D. E. ; Saunders, A. M. ; Strittmatter, W. J. ; Crain, B. J. ; Hulette, C. M. ; Joo, S. H. ; Pericak-Vance, M. A. ; Goldgaber, D. ; Roses, A. D. / Increased amyloid β-peptide deposition in cerebral cortex as a consequence of apolipoprotein E genotype in late-onset Alzheimer disease. In: Proceedings of the National Academy of Sciences of the United States of America. 1993 ; Vol. 90, No. 20. pp. 9649-9653.
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