Donald E. Schmechel1, Ann M. Saunders1, Warren J. Strittmatter1, Barbara J. Crain1, Christine M. Hulette1, Sun Hyung Joo1, Margaret A. Pericak‐Vance1, Dmitry Goldgaber1, Tommy Martinsson1
1Department of Medicine (Neurology), Duke University Medical Center, Durham, NC 27710.
Tóm tắt
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.
