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.