Parkinson disease (PD) is a degenerative disorder of the central nervous system resulting from depletion of dopaminergic neurons and currently remains incurable despite enormous international research efforts. The development of induced pluripotent stem cell (iPSC) technology opened up the unique possibility of studying disease mechanisms in human tissue that was otherwise not accessible, such as the brain. Of particular interest are the monogenetic forms of PD as they closely resemble the more common ‘idiopathic’ PD and, through the mutated protein, provide a clear research target in iPSC-derived neurons. Recessively inherited Parkin and PTEN-induced putative kinase 1 (PINK1) mutations have been investigated in this context and the present review describes the first insights gained from studies in iPSC-derived dopaminergic neurons, which comprise abnormalities in mitochondrial and dopamine homoeostasis, microtubular stability and axonal outgrowth. These new models of PD have a high translational potential that includes the identification of druggable targets, testing of known and novel therapeutic agents in the disease-relevant tissue using well-defined read-outs and potential regenerative approaches.
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April 2015
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Conference Article|
April 07 2015
iPS models of Parkin and PINK1
Aleksandar Rakovic;
Aleksandar Rakovic
*Institute of Neurogenetics, University of Lübeck, Lübeck, Germany
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Philip Seibler;
Philip Seibler
*Institute of Neurogenetics, University of Lübeck, Lübeck, Germany
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Christine Klein
Christine Klein
1
*Institute of Neurogenetics, University of Lübeck, Lübeck, Germany
1To whom correspondence should be addressed (emailchristine.klein@neuro.uni-luebeck.de).
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Publisher: Portland Press Ltd
Received:
January 12 2015
Online ISSN: 1470-8752
Print ISSN: 0300-5127
© The Authors Journal compilation © 2015 Biochemical Society
2015
Biochem Soc Trans (2015) 43 (2): 302–307.
Article history
Received:
January 12 2015
Citation
Aleksandar Rakovic, Philip Seibler, Christine Klein; iPS models of Parkin and PINK1. Biochem Soc Trans 1 April 2015; 43 (2): 302–307. doi: https://doi.org/10.1042/BST20150010
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