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galanthamine/nausea

Krækjan er vistuð á klemmuspjaldið
GreinarKlínískar rannsóknirEinkaleyfi
6 niðurstöður

[Galanthamine versus donepezil in the treatment of Alzheimer's disease].

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OBJECTIVE To use comparative studies on the utilisation of the acetylcholinesterase inhibitors (AchE), galanthamine and donepezil, to evaluate the effectiveness and tolerance of the two drugs in the treatment of the symptoms of Alzheimer's disease (AD). METHODS A search was conducted on Medline for
BACKGROUND The purpose of the study was to determine the possible effect of the cholinesterase inhibitor, galanthamine, on cognition when administered to antagonise neuromuscular blockade after anaesthesia. METHODS The Wechsler Memory Scale was used to assess cognition before and after cataract

Review of the acetylcholinesterase inhibitor galanthamine.

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Galanthamine (or galantamine, Reminyl) is a tertiary alkaloid acetylcholinesterase inhibitor (AChEI) which has been approved in several countries for the symptomatic treatment of senile dementia of the Alzheimer's type. Derived from bulbs of the common snowdrop and several Amaryllidaceae plants,

Galanthamine.

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Galanthamine is a selective acetylcholinesterase inhibitor which has shown potential for the treatment of Alzheimer's disease. Galanthamine is selective for acetylcholinesterase versus butyrylcholinesterase; however, the drug produces greater enzyme inhibition in human erythrocytes than in human

Acetylcholinesterase inhibitors from the toadstool Cortinarius infractus.

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Inhibition of acetylcholinesterase (AChE) and therefore prevention of acetylcholine degradation is one of the most accepted therapy opportunities for Alzheimer s disease (AD), today. Due to lack of selectivity of AChE inhibitor drugs on the market, AD-patients suffer from side effects like nausea or

Cholinesterase inhibitors in the treatment of Alzheimer's disease: a comparison of tolerability and pharmacology.

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Cholinesterase inhibitors are currently the most established treatment strategy in Alzheimer's disease. The treatment effect appears mainly to be symptomatic. Effects on progression of the disease following long term treatment, and possible neuroprotective effects, have been investigated. Delay
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