Abstract: Processes for detecting compounds which protect against fluorescent light-induced DNA lesions, in particular DNA lesions which are induced by oxygen free radicals, are disclosed. The methods of the present invention encompass modifying G.sub.1 -phase test and/or G.sub.2 -phase tests so that a compound which is suspected of being capable of protecting against the formation of fluorescent light-induced DNA lesions (i.e., a suspected "DNA protectant"), such as an anti-oxidant or free-radical scavenger, is added to the cell cultures prior to irradiation of the cell cultures with fluorescent light or x-rays. Addition of a DNA protectant to cultures of human skin fibroblasts or PHA-stimulated blood lymphocytes significantly reduces the frequency of radiation-induced chromatid breaks so that there is a small, preferably no, statistical difference in the frequency of radiation-induced chromatid breaks in Alzheimer disease cells in the presence or absence of caffeine in the G.sub.

Abstract: A process for aiding in the diagnosis of Alzheimer disease is disclosed in which the frequency of chromatid breaks and gaps is calculated in G.sub.1 -phase fluorescent-light-irradiated skin fibroblasts or stimulated peripheral blood lymphocytes after the addition of the DNA repair inhibitor caffeine or in G.sub.2 -phase fluorescent-light-irradiated skin fibroblasts or stimulated peripheral blood lymphocytes after the addition of the DNA repair inhibitor 1.beta.-D-arabinofuranosylcytosine (ara-C). In the G.sub.1 -phase test, the presence of Alzheimer disease is indicated when the total frequency of breaks and gaps caused by caffeine in the cells being examined is higher than the total frequency caused by caffeine in the normal cells. In the G.sub.2 -phase test, the presence of Alzheimer disease is indicated when the total frequency of breaks and gaps in the presence of ara-C is much less in the cells being examined than in normal cells.