dc.contributor.author |
Vives-Bauzà, Cristòfol |
|
dc.contributor.author |
Przedborski, Serge |
|
dc.date.accessioned |
2019-01-16T14:52:25Z |
|
dc.date.available |
2019-01-16T14:52:25Z |
|
dc.identifier.uri |
http://hdl.handle.net/11201/148795 |
|
dc.description.abstract |
[eng] Parkinson's disease (PD) is a common neurodegenerative disorder of unknown cause. Some familial forms of PD are provoked by mutations in the genes encoding for the PTEN (phosphatase and tensin homolog)-induced putative kinase-1 (PINK1) and Parkin. Mounting evidence indicates that PINK1 and Parkin might function in concert to modulate mitochondrial degradation, termed mitophagy. However, the molecular mechanisms by which PINK1/Parkin affect mitophagy are just beginning to be elucidated. Herein, we review the main advances in our understanding of the PINK1/Parkin pathway. Because of the phenotypic similarities among the different forms of PD, a better understanding of PINK1/Parkin biology might have far-reaching pathogenic and therapeutic implications for both the inherited and the sporadic forms of PD. |
|
dc.format |
application/pdf |
|
dc.relation.isformatof |
https://doi.org/10.1016/j.molmed.2010.11.002 |
|
dc.relation.ispartof |
Trends in Molecular Medicine, 2010, vol. 17, num. 3, p. 158-165 |
|
dc.rights |
, 2010 |
|
dc.subject.classification |
57 - Biologia |
|
dc.subject.other |
57 - Biological sciences in general |
|
dc.title |
Mitophagy: the latest problem for Parkinson's disease |
|
dc.type |
info:eu-repo/semantics/article |
|
dc.date.updated |
2019-01-16T14:52:25Z |
|
dc.rights.accessRights |
info:eu-repo/semantics/openAccess |
|
dc.identifier.doi |
https://doi.org/10.1016/j.molmed.2010.11.002 |
|