McCaddon, AndrewBleenow, KajHudson, Peter R.Hughes, AlanBarber, JoanGray, RobDavies, Gareth K.Williams, John H. H.Duguid, JenniferLloyd, AlwynTandy, SteveEverall, MargeCattell, HowardMcCaddon, AnneEllis, DickPalmer, MonaBogdanovic, NenadGottfires, Carl-GerhardZetterberg, HenrikRymo, LarsRegland, Björn2009-06-152009-06-152004-03-17McCaddon, A., Bleenow, K., Hudson, P. R., Hughes, A., Barber, J., Gray, R., Davies, G. K., Williams, J. H. H., Duguid, J., Lloyd, A., Tandy, S., Everall, M., Cattell, H., McCaddon, A., Ellis, D., Palmer, M., Bogdanovic, N., Gottfires, C-G., Zetterberg, H., ... Regland, B. (2004). Transcobalamin polymorphism and serum holo-transcobalamin in relation to Alzheimer's disease. Dementia and Geriatric Cognitive Disorders, 17(3), 215-221. https://doi.org/10.1159/0000763591420-800810.1159/000076359http://hdl.handle.net/10034/70457This article is not available through ChesterRep.Isoforms of the vitamin B<12< carrier protein transcobalamin (TC) might influence its cellular availability and contribute to the association between disrupted single-carbon metabolism and Alzheimer's disease (AD). We therefore investigated the relationships between the TC 776C>G (Pro259Arg) genetic polymorphism, total serum cobalamin and holo-TC levels, and disease onset in 70 patients with clinically diagnosed AD and 74 healthy elderly controls. TC 776C>G polymorphism was also determined for 94 histopathologically confirmed AD patients and 107 controls. Serum holo-TC levels were significantly higher in TC 776C homozygotes (p = 0.04). Kaplan-Meier survival functions differed between homozygous genotypes (Cox's F-Test F(42, 46) = 2.1; p = 0.008) and between 776C homozygotes and heterozygotes (Cox's F test F(46, 108) = 1.7; p = 0.02). Proportionately fewer TC 776C homozygotes appear to develop AD at any given age, but this will require confirmation in a longitudinal study.envitamin B12Alzheimer's diseaseholo-transcobaliaminArticleDementia and Geriatric Cognitive Disorders