scholarly journals Coenzyme Q Induces Nigral Mitochondrial Uncoupling and Prevents Dopamine Cell Loss in a Primate Model of Parkinson’s Disease

Endocrinology ◽  
2003 ◽  
Vol 144 (7) ◽  
pp. 2757-2760 ◽  
Author(s):  
Tamas L. Horvath ◽  
Sabrina Diano ◽  
Csaba Leranth ◽  
Luis Miguel Garcia-Segura ◽  
Michael A. Cowley ◽  
...  

Abstract Parkinson’s disease is characterized by dopamine cell loss of the substantia nigra. Parkinson’s disease and the neurotoxin 1-methyl-4-phenyl-1,2,5,6 tetrahydropyridine may destroy dopamine neurons through oxidative stress. Coenzyme Q is a cofactor of mitochondrial uncoupling proteins that enhances state-4 respiration and eliminate superoxides. Here we report that short-term oral administration of coenzyme Q induces nigral mitochondrial uncoupling and prevents dopamine cell loss after 1-methyl-4-phenyl-1,2,5,6 tetrahydropyridine administration in monkeys.

2018 ◽  
Vol 304 ◽  
pp. 143-153 ◽  
Author(s):  
Claude Rouillard ◽  
Joanie Baillargeon ◽  
Brigitte Paquet ◽  
Michel St-Hilaire ◽  
Jérôme Maheux ◽  
...  

2015 ◽  
Vol 16 (3) ◽  
pp. 269-274 ◽  
Author(s):  
Penelope J. Hallett ◽  
Michela Deleidi ◽  
Arnar Astradsson ◽  
Gaynor A. Smith ◽  
Oliver Cooper ◽  
...  

2001 ◽  
Vol 169 (1) ◽  
pp. 163-181 ◽  
Author(s):  
Manuel Rodrı́guez ◽  
Pedro Barroso-Chinea ◽  
Patricio Abdala ◽  
José Obeso ◽  
Tomás González-Hernández

NeuroImage ◽  
2012 ◽  
Vol 59 (4) ◽  
pp. 3339-3346 ◽  
Author(s):  
Esther Aarts ◽  
Rick C. Helmich ◽  
Marcel J.R. Janssen ◽  
Wim J.G. Oyen ◽  
Bastiaan R. Bloem ◽  
...  

2016 ◽  
Vol 89 ◽  
pp. 55-64 ◽  
Author(s):  
Ludovico Arcuri ◽  
Riccardo Viaro ◽  
Simone Bido ◽  
Francesco Longo ◽  
Mariangela Calcagno ◽  
...  

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Abeer Dagra ◽  
Douglas R. Miller ◽  
Min Lin ◽  
Adithya Gopinath ◽  
Fatemeh Shaerzadeh ◽  
...  

AbstractPathophysiological damages and loss of function of dopamine neurons precede their demise and contribute to the early phases of Parkinson’s disease. The presence of aberrant intracellular pathological inclusions of the protein α-synuclein within ventral midbrain dopaminergic neurons is one of the cardinal features of Parkinson’s disease. We employed molecular biology, electrophysiology, and live-cell imaging to investigate how excessive α-synuclein expression alters multiple characteristics of dopaminergic neuronal dynamics and dopamine transmission in cultured dopamine neurons conditionally expressing GCaMP6f. We found that overexpression of α-synuclein in mouse (male and female) dopaminergic neurons altered neuronal firing properties, calcium dynamics, dopamine release, protein expression, and morphology. Moreover, prolonged exposure to the D2 receptor agonist, quinpirole, rescues many of the alterations induced by α-synuclein overexpression. These studies demonstrate that α-synuclein dysregulation of neuronal activity contributes to the vulnerability of dopaminergic neurons and that modulation of D2 receptor activity can ameliorate the pathophysiology. These findings provide mechanistic insights into the insidious changes in dopaminergic neuronal activity and neuronal loss that characterize Parkinson’s disease progression with significant therapeutic implications.


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