(3H)hemicholinium-3 binding sites in postmortem brains of human patients with Alzheimer's disease and multi-infarct dementia
Language English Country Great Britain, England Media print
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
8591807
DOI
10.1016/0531-5565(94)00062-x
PII: 053155659400062X
Knihovny.cz E-resources
- MeSH
- Alzheimer Disease metabolism MeSH
- Analysis of Variance MeSH
- Choline metabolism MeSH
- Hemicholinium 3 metabolism MeSH
- Binding, Competitive MeSH
- Middle Aged MeSH
- Humans MeSH
- Dementia, Multi-Infarct metabolism MeSH
- Autopsy MeSH
- Aged, 80 and over MeSH
- Aged MeSH
- Case-Control Studies MeSH
- Tritium MeSH
- Binding Sites MeSH
- Check Tag
- Middle Aged MeSH
- Humans MeSH
- Male MeSH
- Aged, 80 and over MeSH
- Aged MeSH
- Female MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Choline MeSH
- Hemicholinium 3 MeSH
- Tritium MeSH
(3H)Hemicholinium-3 ((3H)HCh-3), a potent, selective, and competitive inhibitor of the high-affinity choline uptake process was used for the detection of high-affinity choline carriers in the hippocampus (gyrus parahippocampalis), neocortex (gyrus frontalis medius), and cerebellum (lobulus semilunaris inferior) in autopsy samples of people with Alzheimer's disease, multi-infarct dementia and from other psychiatric and nonpsychiatric patients. The effect of postmortem delay was eliminated by means of the cerebellum used as an individual standard. The density of (3H)HCh-3 binding sites was decreased in the hippocampus and neocortex from individuals with multi-infarct dementia and unchanged in the brain tissue from people with Alzheimer's disease in comparison with control patients. No changes in dissociation constants were found. In Alzheimer's disease, high-affinity choline transport appears to be reduced by a dysfunction of cholinergic neuronal membrane rather than by a significant decrease in the number of presynaptic cholinergic nerve terminals. Results provide evidence of a decrease in the number of nerve endings in people with multi-infarct dementia and suggest different vulnerability of particular brain areas to vascular disorders.
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