Deficient repair of DNA lesions in Alzheimer's disease fibroblasts.
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.
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D000368:Aged; D000544:Alzheimer Disease / Q000235:genetics*; D001761:Bleomycin / Q000494:pharmacology; D002470:Cell Survival; D004260:DNA Repair; D005347:Fibroblasts / Q000187:drug effects / Q000378:metabolism; D006801:Humans; D008769:Methylnitronitrosoguanidine / Q000494:pharmacology; D008875:Middle Aged; D013997:Time Factors
D001761:Bleomycin; D008769:Methylnitronitrosoguanidine