Deficient repair of DNA lesions in Alzheimer's disease fibroblasts.

Journal Article (Academic article)

DNA strand breaks, resulting from treatment with N-methyl-N'-nitro-N-nitrosoguanidine, were repaired more slowly in four strains of familial Alzheimer's disease fibroblasts than in five strains of fibroblasts from age-matched normals. These results were not due to differences between the two cell types in in vitro ages, in the initial DNA damage or in drug-induced cell lysis. Bleomycin-induced DNA double-strand breaks were repaired equally efficiently by both types of cells. Alzheimer's disease cells may have a DNA repair defect, which may be involved in the pathogenesis of this disease.

Duke Authors

Cited Authors

  • Li, JC; Kaminskas, E

Published Date

  • June 1, 1985

Published In

Volume / Issue

  • 129 / 3

Start / End Page

  • 733 - 738

International Standard Serial Number (ISSN)

  • 0006-291X

Conference Location

  • united states