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Nature: A Substantial Source of Auspicious Substances with Acetylcholinesterase Inhibitory Action

Acetylcholinesterase (AChE) (EC 3.1.1.7) is an important enzyme that breaks down of acetylcholine in synaptic cleft in neuronal junctions. Inhibition of AChE is associated with treatment of several diseases such as Alzheimer’s disease (AD), myasthenia gravis, and glaucoma as well as the mechanisms o...

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Autor principal: Orhan, Ilkay Erdogan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Bentham Science Publishers 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3744902/
https://www.ncbi.nlm.nih.gov/pubmed/24381529
http://dx.doi.org/10.2174/1570159X11311040003
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author Orhan, Ilkay Erdogan
author_facet Orhan, Ilkay Erdogan
author_sort Orhan, Ilkay Erdogan
collection PubMed
description Acetylcholinesterase (AChE) (EC 3.1.1.7) is an important enzyme that breaks down of acetylcholine in synaptic cleft in neuronal junctions. Inhibition of AChE is associated with treatment of several diseases such as Alzheimer’s disease (AD), myasthenia gravis, and glaucoma as well as the mechanisms of insecticide and anthelmintic drugs. Several AChE inhibitors are available in clinical use currently for the treatment of AD; however, none of them has ability, yet, to seize progress of the disease. Consequently, an extensive research has been going on finding new AChE inhibitors. In this sense, natural inhibitors have gained great attention due to their encouraging effects toward AChE. In this review, promising candidate molecules with marked AChE inhibition from both plant and animal sources will be underlined.
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spelling pubmed-37449022014-01-01 Nature: A Substantial Source of Auspicious Substances with Acetylcholinesterase Inhibitory Action Orhan, Ilkay Erdogan Curr Neuropharmacol Article Acetylcholinesterase (AChE) (EC 3.1.1.7) is an important enzyme that breaks down of acetylcholine in synaptic cleft in neuronal junctions. Inhibition of AChE is associated with treatment of several diseases such as Alzheimer’s disease (AD), myasthenia gravis, and glaucoma as well as the mechanisms of insecticide and anthelmintic drugs. Several AChE inhibitors are available in clinical use currently for the treatment of AD; however, none of them has ability, yet, to seize progress of the disease. Consequently, an extensive research has been going on finding new AChE inhibitors. In this sense, natural inhibitors have gained great attention due to their encouraging effects toward AChE. In this review, promising candidate molecules with marked AChE inhibition from both plant and animal sources will be underlined. Bentham Science Publishers 2013-07 2013-07 /pmc/articles/PMC3744902/ /pubmed/24381529 http://dx.doi.org/10.2174/1570159X11311040003 Text en ©Bentham Science Publishers http://creativecommons.org/licenses/by/2.5/ This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.5/), which permits unrestrictive use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Article
Orhan, Ilkay Erdogan
Nature: A Substantial Source of Auspicious Substances with Acetylcholinesterase Inhibitory Action
title Nature: A Substantial Source of Auspicious Substances with Acetylcholinesterase Inhibitory Action
title_full Nature: A Substantial Source of Auspicious Substances with Acetylcholinesterase Inhibitory Action
title_fullStr Nature: A Substantial Source of Auspicious Substances with Acetylcholinesterase Inhibitory Action
title_full_unstemmed Nature: A Substantial Source of Auspicious Substances with Acetylcholinesterase Inhibitory Action
title_short Nature: A Substantial Source of Auspicious Substances with Acetylcholinesterase Inhibitory Action
title_sort nature: a substantial source of auspicious substances with acetylcholinesterase inhibitory action
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3744902/
https://www.ncbi.nlm.nih.gov/pubmed/24381529
http://dx.doi.org/10.2174/1570159X11311040003
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