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Article in English | MEDLINE | ID: mdl-12551727

ABSTRACT

Alzheimer's disease (AD) is known to be characterised by a decrease in several brain neurotransmitters. However, the neurotransmitter, which decreases most markedly in this disorder, is acetylcholine (Ach). In addition, the biosynthetic enzyme for Ach, viz. choline acetyltransferase, is also decreased significantly. The ultimate loss of cholinergic neurons and subsequent neurodegeneration in this disorder is thought to be due to free radicals. Presently, there are no reports on the neuroprotective effects of Ach. If Ach has neuroprotective effects, its decline could leave the brain exposed to insults such as free radical damage. Thus, in the present study, the authors determined the ability of Ach to scavenge free radicals using the nitroblue tetrazolium (NBT) assay and also examined its ability to inhibit KCN-induced lipid peroxidation in rat brain homogenates. The results show that Ach inhibits the KCN-induced rise in free radicals and lipid peroxidation. Thus, Ach appears to have neuroprotective properties and this could thus be one reason for the acceleration in neurodegeneration once the levels of this neurotransmitter decline in AD.


Subject(s)
Acetylcholine/pharmacology , Free Radical Scavengers , Lipid Peroxidation , Superoxides , Alzheimer Disease/physiopathology , Alzheimer Disease/prevention & control , Animals , Brain/physiology , Disease Models, Animal , Enzyme Inhibitors/pharmacology , Male , Neuroprotective Agents/pharmacology , Potassium Cyanide/pharmacology , Rats , Rats, Wistar
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