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.

Keywords

Apolipoprotein ESenile plaquesAlzheimer's diseaseAlleleCerebral cortexAmyloid betaGenotypeDegenerative diseasePathologyBETA (programming language)Amyloid (mycology)BiologyInternal medicineEndocrinologyMedicineDiseaseGeneGenetics

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Year
1993
Type
article
Volume
90
Issue
20
Pages
9649-9653
Citations
1509
Access
Closed

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D. E. Schmechel, Ann M. Saunders, Warren J. Strittmatter et al. (1993). 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 , 90 (20) , 9649-9653. https://doi.org/10.1073/pnas.90.20.9649

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DOI
10.1073/pnas.90.20.9649