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Serum cobalamin and methylmalonic acid in Alzheimer dementia
Author(s) -
Kristensen M. Ø.,
Gulmann N. C.,
Christensen J. E. J.,
Østergaard K.,
Rasmussen K.
Publication year - 1993
Publication title -
acta neurologica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.967
H-Index - 95
eISSN - 1600-0404
pISSN - 0001-6314
DOI - 10.1111/j.1600-0404.1993.tb04140.x
Subject(s) - cobalamin , methylmalonic acid , dementia , medicine , alzheimer's disease , metabolite , hydroxocobalamin , homocysteine , endocrinology , cyanocobalamin , vitamin b12 , gastroenterology , disease
The cobalamin status was evaluated in Alzheimer dementia (n = 26), other dementias (n = 24), various gerontopsychiatric disorders (n = 25), and in neuropsychiatrically healthy controls (n = 20). Supplementing serum cobalamin we measured methylmalonic acid (MMA), a metabolite accumulating early in cobalamin deficiency. Subnormal cobalamin and/or clearly elevated MMA concentrations were found in 11 cases: 7 Alzheimer patients (27%), 2 with other dementias (8%), one psychiatric patient (4%), and one control (5%). None presented the typical neurologic features of cobalamin deficiency and macrocytosis was found in only one. The mean cobalamin concentration was significantly lower in Alzheimer patients (179 ± 18 pmol/1) than in the age‐matched controls (256 ± 23 pmol/1) (p = 0.013) and the other patient groups. Correspondingly, the mean MMA level was higher in the Alzheimer group (0.480 ± 0.062 μmol/1) than in any other diagnostic group (controls: 0.347 ± 0.040 μmol/1). Comparing the Alzheimer group to the other groups as a whole, the elevation was significant (p = 0.0097). Our findings indicate that Alzheimer patients are particularly prone to cobalamin deficiency, and even subtle biochemical signs of deficiency seem to justify treatment.