Apolipoprotein E genotype and Lewy body disease

C. F. Lippa, T. W. Smith, A. M. Saunders, R. Crook, D. Pulaski-Salo, P. Davies, J. Hardy, A. D. Roses, D. Dickson

Research output: Contribution to journalArticlepeer-review

89 Scopus citations


To determine whether apolipoprotein E (APOE) genotype affects neuropathology in Lewy body disease (LBD), we examined 18 cases of LBD that did not have concurrent Alzheimer's disease by the CERAD criteria. We obtained APOE genotypes, determined diffuse β-amyloid plaque (AβP) and Lewy body densities in multiple brain regions, and graded the intensity of CA2-3 ubiquitin-positive neurites, vacuolar change, nigral pathology, amyloid angiopathy, and subpial amyloid deposition. The APOE allele frequencies were as follows: ε2, 0.14 ± 0.07; ε3, 0.64 ± 0.08; and ε4, 0.22 ± 0.03. The mean AβP density was lower in APOE ε3/3 cases (14.5 AβPs per mm2) than in the groups with the APOE ε2 (67.0) or APOE ε4 (46.6) alleles. This difference was due largely to the difference between AβP density in the APOE ε2 group and the APOE ε3/3 group (F = 5.525, p < 0.02). CA2-3 neuritic degeneration was greater in those with the APOE ε4 allele than in those with the APOE ε3/3 genotype (grade = 1.9 ± 1.3 versus 0.938 ± 0.9; Kruskal- Wallis test statistic = 6.962, p < 0.05). These data are consistent with the hypothesis that APOE genotype may affect neuropathology in LBD.

Original languageEnglish (US)
Pages (from-to)97-103
Number of pages7
Issue number1
StatePublished - Jan 1995

ASJC Scopus subject areas

  • Clinical Neurology


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