INCREASED AMYLOID BETA-PEPTIDE DEPOSITION IN CEREBRAL-CORTEX AS A CONSEQUENCE OF APOLIPOPROTEIN-E GENOTYPE IN LATE-ONSET ALZHEIMER-DISEASE

Citation
De. Schmechel et al., INCREASED AMYLOID BETA-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 Statesof America, 90(20), 1993, pp. 9649-9653
Citations number
39
Categorie Soggetti
Multidisciplinary Sciences
ISSN journal
00278424
Volume
90
Issue
20
Year of publication
1993
Pages
9649 - 9653
Database
ISI
SICI code
0027-8424(1993)90:20<9649:IABDIC>2.0.ZU;2-H
Abstract
Amyloid beta-peptide (Abeta) deposition in senile plaques and cerebral vessels is a neuropathological feature of Alzheimer disease (AD). We examined the possibility that commonly observed variability in Abeta d eposition in late-onset AD might be related to apolipoprotein E genoty pe (APOE gene; the two most common alleles are 3 and 4), since APOE4 i s a susceptibility gene for late-onset AD and apolipoprotein E interac ts strongly with Abeta in vitro. In an autopsy series of brains of lat e-onset AD patients, we found a strong association of APOE4 allele wit h increased vascular and plaque Abeta deposits. Late-onset AD patients with one or two APOE4 alleles have a distinct neuropathological pheno type compared with patients homozygous for APOE3.