The transport of 57Co-B 12 from plasma into brain of 6-hydroxydopa treated rats: Implications for the use of vitamin B 12 therapy in Alzheimer's Dementia

Abstract

It has been suggested that the deficient vitamin B 12 transport into brain tissue which is commonly observed in patients with Alzheimer's Dementia is produced by deficient noradrenergic neurotransmission. To determine the effects of central noradrenergic depletion on the transport of vitamin B 12 into brain tissue, rats were injected (i.p.) with 57Co labelled vitamin B 12 several days after their central noradrenergic neurons were destroyed with injections of 6-hydroxydopa. Pretreatment with this neurotoxin did not alter the passage of 57Co-B 12 into the brain, and we conclude that the noradrenergic/vitamin B 12 transport mechanism is not of primary significance in Alzheimer's Dementia. Other mechanisms involving impaired microsomal liver enzyme function may be more important in the aetiology of Alzheimer's Dementia.