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

Abstract

Article abstract-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 beta-amyloid plaque (AbetaP) 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: epsilon2, 0.14 +\- 0.07; epsilon3, 0.64 +\- 0.08; and epsilon4, 0.22 +\- 0.03. The mean AbetaP density was lower in APOE epsilon3/3 cases (14.5 AbetaPs per mm2) than in the groups with the APOE epsilon2 (67.0) or APOE epsilon4 (46.6) alleles. This difference was due largely to the difference between AbetaP density in the APOE epsilon2 group and the APOE epsilon3/3 group (F = 5.525, p < 0.02). CA2-3 neuritic degeneration was greater in those with the APOE epsilon4 allele than in those with the APOE epsilon3/3 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
JournalNeurology
Volume45
Issue number1
DOIs
StatePublished - Jan 1995

ASJC Scopus subject areas

  • Clinical Neurology

Fingerprint Dive into the research topics of 'Apolipoprotein e genotype and lewy body disease'. Together they form a unique fingerprint.

Cite this