Effect of 5-alpha reductase inhibitors in animal models of Parkinson's disease.

5alpha-reductase Brain Dopamine Dutasteride Dyskinesia Finasteride Gut Inflammation Neuroprotection Parkinson’s disease

Journal

Frontiers in neuroendocrinology
ISSN: 1095-6808
Titre abrégé: Front Neuroendocrinol
Pays: United States
ID NLM: 7513292

Informations de publication

Date de publication:
29 Sep 2024
Historique:
received: 03 06 2024
revised: 12 09 2024
accepted: 27 09 2024
medline: 3 10 2024
pubmed: 3 10 2024
entrez: 1 10 2024
Statut: aheadofprint

Résumé

Parkinson's disease (PD) is characterized by motor symptoms due to loss of brain dopamine and non-motor symptoms, including gastrointestinal disorders. Although there is no cure for PD, symptomatic treatments are available. L-Dopa is the gold standard PD therapy, but most patients develop dyskinesias (LID), which are challenging to manage. Amantadine is recognized as the most effective drug for LID, but its adverse effects limit the use in patients. Here we review how 5α-reductase inhibitors (5ARIs), drugs used to treat benign prostatic hyperplasia and alopecia, exhibit beneficial effects in PD animal models. 5ARIs show neuroprotective properties in brain and gut dopaminergic systems, and reduce dyskinesias in rodent model of PD. Additionally, the 5ARI finasteride dampened dopaminergic-induced drug gambling in PD patients. Neuroprotection and antidyskinetic activities of 5ARIs in animal models of PD suggest their potential repurposing in men with PD to address gut dysfunction, protect brain DA and inhibit dyskinesias.

Identifiants

pubmed: 39353534
pii: S0091-3022(24)00036-0
doi: 10.1016/j.yfrne.2024.101156
pii:
doi:

Types de publication

Journal Article Review

Langues

eng

Sous-ensembles de citation

IM

Pagination

101156

Informations de copyright

Copyright © 2024 The Author(s). Published by Elsevier Inc. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Auteurs

Mélanie Bourque (M)

Axe Neurosciences, Centre de recherche du CHU de Québec-Université Laval, Québec, QC, Canada; Faculty of Pharmacy, Laval University, Quebec, QC, Canada.

Marc Morissette (M)

Axe Neurosciences, Centre de recherche du CHU de Québec-Université Laval, Québec, QC, Canada; Faculty of Pharmacy, Laval University, Quebec, QC, Canada.

Amandine Isenbrandt (A)

Axe Neurosciences, Centre de recherche du CHU de Québec-Université Laval, Québec, QC, Canada; Faculty of Pharmacy, Laval University, Quebec, QC, Canada.

Silvia Giatti (S)

Department of Pharmacological and Biomolecular Sciences, Center of Excellence on Neurodegenerative Diseases, Università degli Studi di Milano, Milan, Italy.

Roberto Cosimo Melcangi (R)

Department of Pharmacological and Biomolecular Sciences, Center of Excellence on Neurodegenerative Diseases, Università degli Studi di Milano, Milan, Italy.

Manolo Carta (M)

Department of Biomedical Sciences, "Guy Everett Laboratory", University of Cagliari, Cittadella Universitaria SP 8, Monserrato 09042, Italy.

Roberto Frau (R)

Department of Biomedical Sciences, "Guy Everett Laboratory", University of Cagliari, Cittadella Universitaria SP 8, Monserrato 09042, Italy.

Marco Bortolato (M)

Department of Pharmacology and Toxicology, College of Pharmacy, University of Utah, 30 S 2000 E, Salt Lake City, UT 84112, USA.

Denis Soulet (D)

Axe Neurosciences, Centre de recherche du CHU de Québec-Université Laval, Québec, QC, Canada; Faculty of Pharmacy, Laval University, Quebec, QC, Canada.

Thérèse Di Paolo (T)

Axe Neurosciences, Centre de recherche du CHU de Québec-Université Laval, Québec, QC, Canada; Faculty of Pharmacy, Laval University, Quebec, QC, Canada. Electronic address: therese.dipaolo@crchudequebec.ulaval.ca.

Classifications MeSH