scholarly journals Molecular mechanisms underlying protective effects of quercetin against mitochondrial dysfunction and progressive dopaminergic neurodegeneration in cell culture and MitoPark transgenic mouse models of Parkinson's Disease

2017 ◽  
Vol 141 (5) ◽  
pp. 766-782 ◽  
Author(s):  
Muhammet Ay ◽  
Jie Luo ◽  
Monica Langley ◽  
Huajun Jin ◽  
Vellareddy Anantharam ◽  
...  
2007 ◽  
Vol 13 ◽  
pp. S90
Author(s):  
S. Nuber ◽  
E. Petrasch-Parwez ◽  
B. Winner ◽  
J. Winkler ◽  
S. von Hörsten ◽  
...  

2007 ◽  
Vol 13 ◽  
pp. S122
Author(s):  
S. Nuber ◽  
E. Petrasch-Parwez ◽  
B. Winner ◽  
J. Winkler ◽  
S. von Hörsten ◽  
...  

1996 ◽  
Vol 252 (4) ◽  
pp. 465-469
Author(s):  
G. Donofrio ◽  
A. J. Clark ◽  
C. B. A. Whitelaw ◽  
G. Donofrio ◽  
E. Bignetti

2011 ◽  
Vol 2011 ◽  
pp. 1-13 ◽  
Author(s):  
Daniela M. Arduíno ◽  
A. Raquel Esteves ◽  
Sandra M. Cardoso

Understanding the molecular basis of Parkinson's disease (PD) has proven to be a major challenge in the field of neurodegenerative diseases. Although several hypotheses have been proposed to explain the molecular mechanisms underlying the pathogenesis of PD, a growing body of evidence has highlighted the role of mitochondrial dysfunction and the disruption of the mechanisms of mitochondrial dynamics in PD and other parkinsonian disorders. In this paper, we comment on the recent advances in how changes in the mitochondrial function and mitochondrial dynamics (fusion/fission, transport, and clearance) contribute to neurodegeneration, specifically focusing on PD. We also evaluate the current controversies in those issues and discuss the role of fusion/fission dynamics in the mitochondrial lifecycle and maintenance. We propose that cellular demise and neurodegeneration in PD are due to the interplay between mitochondrial dysfunction, mitochondrial trafficking disruption, and impaired autophagic clearance.


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