Vitamin B12-induced reduction of platelet monoamine oxidase activity in patients with dementia and pernicious anaemia.
Platelet monoamine oxidase (MAO) activity has previously been shown to be increased in patients with senile dementia of Alzheimer type (SDAT) and in patients with megaloblastic anaemia. Moreover, low serum B12 levels were found to be 4-5 times more frequent in SDAT compared with an unselected population of similar age. In the present investigation, platelet MAO activity was estimated in 14 SDAT patients with relatively low serum B12 levels and in 4 patients with pernicious anaemia. Before B12 therapy, platelet MAO activity was significantly increased in both patient groups compared with a control group. After B12 therapy, platelet MAO activity was significantly reduced in both patient groups to apparently normal levels. The present results show that B12 status is a controlling factor of platelet MAO activity and confirm that a significant connection exists between vitamin B12 deficiency and primary degenerative dementia disorders, such as SDAT.
Regland
B
B
Department of Psychiatry, St. Jörgen's Hospital, University of Gothenburg, Sweden.
Gottfries
C G
CG
Oreland
L
L
D000368:Aged; D000544:Alzheimer Disease / Q000201:enzymology*; D000752:Anemia, Pernicious / Q000188:drug therapy / Q000201:enzymology*; D001792:Blood Platelets / Q000187:drug effects / Q000201:enzymology*; D005260:Female; D006801:Humans; D006879:Hydroxocobalamin / Q000008:administration & dosage*; D007273:Injections, Intramuscular; D008297:Male; D008995:Monoamine Oxidase / Q000097:blood*; D014805:Vitamin B 12 / Q000097:blood; D014806:Vitamin B 12 Deficiency / Q000188:drug therapy / Q000201:enzymology*
D008995:Monoamine Oxidase; D014805:Vitamin B 12; D006879:Hydroxocobalamin