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Deficits in cholinergic neurotransmission and their clinical correlates in Parkinson’s disease

In view of its ability to explain the most frequent motor symptoms of Parkinson’s Disease (PD), degeneration of dopaminergic neurons has been considered one of the disease’s main pathophysiological features. Several studies have shown that neurodegeneration also affects noradrenergic, serotoninergic...

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Autores principales: Perez-Lloret, Santiago, Barrantes, Francisco J
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5516588/
https://www.ncbi.nlm.nih.gov/pubmed/28725692
http://dx.doi.org/10.1038/npjparkd.2016.1
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author Perez-Lloret, Santiago
Barrantes, Francisco J
author_facet Perez-Lloret, Santiago
Barrantes, Francisco J
author_sort Perez-Lloret, Santiago
collection PubMed
description In view of its ability to explain the most frequent motor symptoms of Parkinson’s Disease (PD), degeneration of dopaminergic neurons has been considered one of the disease’s main pathophysiological features. Several studies have shown that neurodegeneration also affects noradrenergic, serotoninergic, cholinergic and other monoaminergic neuronal populations. In this work, the characteristics of cholinergic deficits in PD and their clinical correlates are reviewed. Important neurophysiological processes at the root of several motor and cognitive functions remit to cholinergic neurotransmission at the synaptic, pathway, and circuital levels. The bulk of evidence highlights the link between cholinergic alterations and PD motor symptoms, gait dysfunction, levodopa-induced dyskinesias, cognitive deterioration, psychosis, sleep abnormalities, autonomic dysfunction, and altered olfactory function. The pathophysiology of these symptoms is related to alteration of the cholinergic tone in the striatum and/or to degeneration of cholinergic nuclei, most importantly the nucleus basalis magnocellularis and the pedunculopontine nucleus. Several results suggest the clinical usefulness of antimuscarinic drugs for treating PD motor symptoms and of inhibitors of the enzyme acetylcholinesterase for the treatment of dementia. Data also suggest that these inhibitors and pedunculopontine nucleus deep-brain stimulation might also be effective in preventing falls. Finally, several drugs acting on nicotinic receptors have proved efficacious for treating levodopa-induced dyskinesias and cognitive impairment and as neuroprotective agents in PD animal models. Results in human patients are still lacking.
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spelling pubmed-55165882017-07-19 Deficits in cholinergic neurotransmission and their clinical correlates in Parkinson’s disease Perez-Lloret, Santiago Barrantes, Francisco J NPJ Parkinsons Dis Review Article In view of its ability to explain the most frequent motor symptoms of Parkinson’s Disease (PD), degeneration of dopaminergic neurons has been considered one of the disease’s main pathophysiological features. Several studies have shown that neurodegeneration also affects noradrenergic, serotoninergic, cholinergic and other monoaminergic neuronal populations. In this work, the characteristics of cholinergic deficits in PD and their clinical correlates are reviewed. Important neurophysiological processes at the root of several motor and cognitive functions remit to cholinergic neurotransmission at the synaptic, pathway, and circuital levels. The bulk of evidence highlights the link between cholinergic alterations and PD motor symptoms, gait dysfunction, levodopa-induced dyskinesias, cognitive deterioration, psychosis, sleep abnormalities, autonomic dysfunction, and altered olfactory function. The pathophysiology of these symptoms is related to alteration of the cholinergic tone in the striatum and/or to degeneration of cholinergic nuclei, most importantly the nucleus basalis magnocellularis and the pedunculopontine nucleus. Several results suggest the clinical usefulness of antimuscarinic drugs for treating PD motor symptoms and of inhibitors of the enzyme acetylcholinesterase for the treatment of dementia. Data also suggest that these inhibitors and pedunculopontine nucleus deep-brain stimulation might also be effective in preventing falls. Finally, several drugs acting on nicotinic receptors have proved efficacious for treating levodopa-induced dyskinesias and cognitive impairment and as neuroprotective agents in PD animal models. Results in human patients are still lacking. Nature Publishing Group 2016-02-18 /pmc/articles/PMC5516588/ /pubmed/28725692 http://dx.doi.org/10.1038/npjparkd.2016.1 Text en Copyright © 2016 Parkinson's Disease Foundation/Macmillan Publishers Limited http://creativecommons.org/licenses/by/4.0/ This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/
spellingShingle Review Article
Perez-Lloret, Santiago
Barrantes, Francisco J
Deficits in cholinergic neurotransmission and their clinical correlates in Parkinson’s disease
title Deficits in cholinergic neurotransmission and their clinical correlates in Parkinson’s disease
title_full Deficits in cholinergic neurotransmission and their clinical correlates in Parkinson’s disease
title_fullStr Deficits in cholinergic neurotransmission and their clinical correlates in Parkinson’s disease
title_full_unstemmed Deficits in cholinergic neurotransmission and their clinical correlates in Parkinson’s disease
title_short Deficits in cholinergic neurotransmission and their clinical correlates in Parkinson’s disease
title_sort deficits in cholinergic neurotransmission and their clinical correlates in parkinson’s disease
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5516588/
https://www.ncbi.nlm.nih.gov/pubmed/28725692
http://dx.doi.org/10.1038/npjparkd.2016.1
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