Analogues, ageing and aberrant assimilation of vitamin B12 in Alzheimer's disease

Citation
A. Mccaddon et al., Analogues, ageing and aberrant assimilation of vitamin B12 in Alzheimer's disease, DEMENT G C, 12(2), 2001, pp. 133-137
Citations number
31
Categorie Soggetti
Neurology,"Neurosciences & Behavoir
Journal title
DEMENTIA AND GERIATRIC COGNITIVE DISORDERS
ISSN journal
14208008 → ACNP
Volume
12
Issue
2
Year of publication
2001
Pages
133 - 137
Database
ISI
SICI code
1420-8008(200103/04)12:2<133:AAAAAO>2.0.ZU;2-4
Abstract
Vitamin B12 assimilation might be disrupted in patients with Alzheimer's di sease. We therefore measured B12 carrier protein saturation and inactive B1 2 'analogues' in patients compared with healthy elderly individuals in a pr ospective case-controlled survey, Twenty-three patients, aged 60 or over, w ith features compatible with DSM-IV criteria for primary degenerative demen tia of the Alzheimer type were recruited together with 18 cognitively intac t age-matched control subjects. Total vitamin B12 (active corrinoids), holo - and apo-haptocorrin and transcobalamin were measured in serum. B12 analog ues (inactive corrinoids) were estimated from the difference between R-bind er-determined corrinoids and an intrinsic factor based B12 assay. Alzheimer patients had significantly lower active corrinoid than control subjects a nd the analogue/corrinoid ratio was significantly higher in the Alzheimer g roup. The inter-relationship between age, analogues and transcobalamin pola rised patients into two distinct groups. Two disparate mechanisms might exi st for the development of cerebral B12 deficiency in Alzheimer's disease, a lthough both imply a disruption of selective B12 assimilation and analogue elimination in such patients. Copyright (C) 2001 S. Karger AG, Basel.