Journal
MOVEMENT DISORDERS
Volume 31, Issue 10, Pages 1433-1443Publisher
WILEY
DOI: 10.1002/mds.26797
Keywords
Parkinson's disease; Atp13a2; Kufor-Rakeb syndrome; endolysosomal system
Categories
Funding
- National Institute of Neurological Diseases and Stroke [R01 NS061098, F31 NS078817, T32 GM007863]
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Increasingly, genetic, cell biological, and in vivo work emphasizes the role of the endolysosomal system dysfunction in Parkinson's disease pathogenesis. Yet many questions remain about the mechanisms by which primary endolysosomal dysfunction causes PD as well as how the endolysosomal system interacts with -synuclein-mediated neurotoxicity. We recently described a new mouse model of parkinsonism in which loss of the endolysosomal protein Atp13a2 causes behavioral, neuropathological, and biochemical changes similar to those present in human subjects with ATP13A2 mutations. In this Scientific Perspectives, we revisit the evidence implicating the endolysosomal system in PD, current hypotheses of disease pathogenesis, and how recent studies refine these hypotheses and raise new questions for future research. (c) 2016 International Parkinson and Movement Disorder Society.
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