Nicotine suppresses Parkinson’s disease like phenotypes induced by Synphilin-1 overexpression in Drosophila melanogaster by increasing tyrosine hydroxylase and dopamine levels

Abstract It has been observed that there is a lower Parkinson’s disease (PD) incidence in tobacco users. Nicotine is a cholinergic agonist and is the principal psychoactive compound in tobacco linked to cigarette addiction. Different studies have shown that nicotine has beneficial effects on sporadi...

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Autores principales: Angel Carvajal-Oliveros, Carmen Domínguez-Baleón, Rafaella V. Zárate, Jorge M. Campusano, Verónica Narváez-Padilla, Enrique Reynaud
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Publicado: Nature Portfolio 2021
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Acceso en línea:https://doaj.org/article/2a4fbd441f2c45dd98e95e3ab2c8c088
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spelling oai:doaj.org-article:2a4fbd441f2c45dd98e95e3ab2c8c0882021-12-02T14:41:56ZNicotine suppresses Parkinson’s disease like phenotypes induced by Synphilin-1 overexpression in Drosophila melanogaster by increasing tyrosine hydroxylase and dopamine levels10.1038/s41598-021-88910-42045-2322https://doaj.org/article/2a4fbd441f2c45dd98e95e3ab2c8c0882021-05-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-88910-4https://doaj.org/toc/2045-2322Abstract It has been observed that there is a lower Parkinson’s disease (PD) incidence in tobacco users. Nicotine is a cholinergic agonist and is the principal psychoactive compound in tobacco linked to cigarette addiction. Different studies have shown that nicotine has beneficial effects on sporadic and genetic models of PD. In this work we evaluate nicotine’s protective effect in a Drosophila melanogaster model for PD where Synphilin-1 (Sph-1) is expressed in dopaminergic neurons. Nicotine has a moderate effect on dopaminergic neuron survival that becomes more evident as flies age. Nicotine is beneficial on fly survival and motility increasing tyrosine hydroxylase and dopamine levels, suggesting that cholinergic agonists may promote survival and metabolic function of the dopaminergic neurons that express Sph-1. The Sph-1 expressing fly is a good model for the study of early-onset phenotypes such as olfaction loss one of the main non-motor symptom related to PD. Our data suggest that nicotine is an interesting therapeutic molecule whose properties should be explored in future research on the phenotypic modulators of the disease and for the development of new treatments.Angel Carvajal-OliverosCarmen Domínguez-BaleónRafaella V. ZárateJorge M. CampusanoVerónica Narváez-PadillaEnrique ReynaudNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-13 (2021)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Angel Carvajal-Oliveros
Carmen Domínguez-Baleón
Rafaella V. Zárate
Jorge M. Campusano
Verónica Narváez-Padilla
Enrique Reynaud
Nicotine suppresses Parkinson’s disease like phenotypes induced by Synphilin-1 overexpression in Drosophila melanogaster by increasing tyrosine hydroxylase and dopamine levels
description Abstract It has been observed that there is a lower Parkinson’s disease (PD) incidence in tobacco users. Nicotine is a cholinergic agonist and is the principal psychoactive compound in tobacco linked to cigarette addiction. Different studies have shown that nicotine has beneficial effects on sporadic and genetic models of PD. In this work we evaluate nicotine’s protective effect in a Drosophila melanogaster model for PD where Synphilin-1 (Sph-1) is expressed in dopaminergic neurons. Nicotine has a moderate effect on dopaminergic neuron survival that becomes more evident as flies age. Nicotine is beneficial on fly survival and motility increasing tyrosine hydroxylase and dopamine levels, suggesting that cholinergic agonists may promote survival and metabolic function of the dopaminergic neurons that express Sph-1. The Sph-1 expressing fly is a good model for the study of early-onset phenotypes such as olfaction loss one of the main non-motor symptom related to PD. Our data suggest that nicotine is an interesting therapeutic molecule whose properties should be explored in future research on the phenotypic modulators of the disease and for the development of new treatments.
format article
author Angel Carvajal-Oliveros
Carmen Domínguez-Baleón
Rafaella V. Zárate
Jorge M. Campusano
Verónica Narváez-Padilla
Enrique Reynaud
author_facet Angel Carvajal-Oliveros
Carmen Domínguez-Baleón
Rafaella V. Zárate
Jorge M. Campusano
Verónica Narváez-Padilla
Enrique Reynaud
author_sort Angel Carvajal-Oliveros
title Nicotine suppresses Parkinson’s disease like phenotypes induced by Synphilin-1 overexpression in Drosophila melanogaster by increasing tyrosine hydroxylase and dopamine levels
title_short Nicotine suppresses Parkinson’s disease like phenotypes induced by Synphilin-1 overexpression in Drosophila melanogaster by increasing tyrosine hydroxylase and dopamine levels
title_full Nicotine suppresses Parkinson’s disease like phenotypes induced by Synphilin-1 overexpression in Drosophila melanogaster by increasing tyrosine hydroxylase and dopamine levels
title_fullStr Nicotine suppresses Parkinson’s disease like phenotypes induced by Synphilin-1 overexpression in Drosophila melanogaster by increasing tyrosine hydroxylase and dopamine levels
title_full_unstemmed Nicotine suppresses Parkinson’s disease like phenotypes induced by Synphilin-1 overexpression in Drosophila melanogaster by increasing tyrosine hydroxylase and dopamine levels
title_sort nicotine suppresses parkinson’s disease like phenotypes induced by synphilin-1 overexpression in drosophila melanogaster by increasing tyrosine hydroxylase and dopamine levels
publisher Nature Portfolio
publishDate 2021
url https://doaj.org/article/2a4fbd441f2c45dd98e95e3ab2c8c088
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