Author
Rivieire S
Date
11/1998
Journal
Int J Geriatr Psychiatry
Abstract
OBJECTIVE: To compare the vitamin C and E plasma levels in patients with Alzheimer’s disease (AD) and to assess the vitamin C intake and nutritional status. DESIGN: Case-control study. Four groups of sex- and age-matched subjects were compared: severe AD and moderate AD, in patients with moderate AD and controls. SETTING: Community and hospitalized patients in the region of Toulouse, France. PARTICIPANTS: Patients with dementia who fulfilled criteria for Alzheimer’s disease: severe Alzheimer group (N = 20), Mini-Mental State Examination (MMSE) score range 0-9; moderate Alzheimer group (N = 24), MMSE 10-23; hospitalized Alzheimer group (N = 9), MMSE 10-23. Control group (N = 19), MMSE 24-30. MEASURES: Plasma vitamin E and C were quantified by HPLC-fluorescence. Consumption of raw and cooked fruit and vegetables was evaluated in order to determine the mean vitamin C intakes. Mini Nutritional Assessment (MNA) and plasma albumin were used to measure nutritional status. RESULTS: Institutionalized and community subjects were analysed separately. MNA scores were normal in home-living Alzheimer subjects with moderate dementia and significantly lower in those with severe disease, despite normal plasma albumin levels. In the home-living Alzheimer subjects, vitamin C plasma levels decreased in proportion to the severity of the cognitive impairment despite similar vitamin C intakes, whereas vitamin E remained stable. The hospitalized Alzheimer subjects had lower MNA scores and albumin levels but normal vitamin C intakes, but their plasma vitamin C was lower than that of community-living subjects. Institutionalized Alzheimer subjects had significantly lower MNA scores but normal vitamin C and albumin levels and vitamin C intakes compared with community-dwelling subjects of similar degree of cognitive impairment. CONCLUSION: Plasma vitamin C is lower in AD in proportion to the degree of cognitive impairment and is not explained by lower vitamin C intake. These results support the hypothesis that oxygen-free radicals may cause damage.
