title: Low plasma vitamin C in Alzheimer patients despite an adequate diet.
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.
  
  
  METHODS
  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.
  
  
  METHODS
  Community and hospitalized patients in the region of Toulouse, France.
  
  
  METHODS
  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.
  
  
  METHODS
  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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Hôpital La Grave-Casselar, Toulouse, France.
authors.forename: S
authors.initials: S
authors.lastname: Rivière
authors.forename: I
authors.initials: I
authors.lastname: Birlouez-Aragon
authors.forename: F
authors.initials: F
authors.lastname: Nourhashémi
authors.forename: B
authors.initials: B
authors.lastname: Vellas
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D000544:Alzheimer Disease / Q000097:blood / Q000175:diagnosis*; D001205:Ascorbic Acid / Q000097:blood*; D001206:Ascorbic Acid Deficiency / Q000097:blood / Q000175:diagnosis*; D005260:Female; D005602:France; D015577:Geriatric Assessment; D006801:Humans; D008297:Male; D008609:Mental Status Schedule; D008875:Middle Aged; D015596:Nutrition Assessment; D012016:Reference Values; D012931:Social Environment; D014810:Vitamin E / Q000097:blood
chemical_list: D014810:Vitamin E; D001205:Ascorbic Acid