Low plasma vitamin C in Alzheimer patients despite an adequate diet
S. Riviere
Bok Engelsk 1998
| Utgitt | 1998
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| Omfang | Side 749- 754
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| Opplysninger | Objective. To compare the vitamin C and E plasma levels in patientswith Alzheimer's disease (AD) and to assess the vitamin C intake andnutritional status.Design. Case-control study. Four groups of sex- and age-matchedsubjects were compared: severe AD and moderate AD, in patients withmoderate AD and controls.Setting. Community and hospitalized patients in the region ofToulouse, France.Participants. Patients with dementia who fulfilled criteria forAlzheimer's disease: severe Alzheimer group (N = 20), Mini-MentalState 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.Measurers. Plasma vitamin E and C were quantified by HPLC-fluorescence. Consumption of raw and cooked fruit and vegetables wasevaluated in order to determine the mean vitamin C intakes. MiniNutritional Assessment (MNA) and plasma albumin were used to measurenutritional status.Results. Institutionalized and community subjects were analysedseparately. MNA scores were normal in home-living Alzheimer subjectswith moderate dementia and significantly lower in those with severedisease, despite normal plasma albumin levels. In the home-livingAlzheimer subjects, vitamin C plasma levels decreased in proportionto the severity of the cognitive impairment despite similar vitamin Cintakes, whereas vitamin E remained stable. The hospitalizedAlzheimer subjects had lower MNA scores and albumin levels but normalvitamin C intakes, but their plasma vitamin C was lower than that ofcommunity-living subjects. Institutionalized Alzheimer subjects hadsignificantly lower MNA scores but normal vitamin C and albuminlevels and vitamin C intakes compared with community-dwellingsubjects of similar degree of cognitive impairment.Conclusion. Plasma vitamin C is lower in AD in proportion to thedegree of cognitive impairment and is not explained by lower vitaminC intake. These results support the hypothesis that oxygen-freeradicals may cause damage. (C) 1998 John Wiley & Sons, Ltd.
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