LOW PLASMA VITAMIN-C IN ALZHEIMER PATIENTS DESPITE AN ADEQUATE DIET

Objective. To compare the vitamin C and E plasma levels in patients wi th Alzheimer's disease (AD) and to assess the vitamin C intake and nut ritional status.Design. Case-control study. Four groups of sex- and ag e-matched subjects were compared: severe AD and moderate AD, in patien ts with moderate AD and controls. Setting. Community and hospitalized patients in the region of Toulouse, France. Participants. Patients wit h dementia who fulfilled criteria for Alzheimer's disease: severe Alzh eimer group (N = 20), Mini-Mental State Examination (MMSE) score range 0-9; moderate Alzheimer group (N = 24), MMSE 10-23; hospitalized Alzh eimer group (N = 9), MMSE 10-23. Control group (N = 19), MMSE 24-30. M easurers. Plasma vitamin E and C were quantified by HPLC-fluorescence. Consumption of raw and cooked fruit and vegetables was evaluated in o rder to determine the mean vitamin C intakes. Mini Nutritional Assessm ent (MNA) and plasma albumin were used to measure nutritional status. Results. Institutionalized and community subjects were analysed separa tely. MNA scores were normal in home-living Alzheimer subjects with mo derate dementia and significantly lower in those with severe disease, despite normal plasma albumin levels. In the home-living Alzheimer sub jects, vitamin C plasma levels decreased in proportion to the severity of the cognitive impairment despite similar vitamin C intakes, wherea s vitamin E remained stable. The hospitalized Alzheimer subjects had l ower MNA scores and albumin levels but normal vitamin C intakes, but t heir plasma vitamin C was lower than that of community-living subjects . Institutionalized Alzheimer subjects had significantly lower MNA sco res but normal vitamin C and albumin levels and vitamin C intakes comp ared with community-dwelling subjects of similar degree of cognitive i mpairment. Conclusion. Plasma vitamin C is lower in AD in proportion t o the degree of cognitive impairment and is not explained by lower vit amin C intake. These results support the hypothesis that oxygen-free r adicals may cause damage. (C) 1998 John Wiley & Sons, Ltd.