The role of ATP13A2/PARK9 in secretion of exosomes and alpha synuclein

Project: Research project

Project Details


While most neurodegenerative disorders are characterized by the accumulation of aggregated mutant proteins primarily in neurons, the contribution of glial cells in this process remains poorly explored. In our recent work, we demonstrated that astrocytes contribute to removal of extracellular a-synuclein and that disruption of this pathway caused by mutations in the Parkinson’s disease-linked gene ATP13A2/PARK9 result in a-synuclein accumulation in human dopaminergic neurons. We found astrocytes also protect neurons from a-synuclein propagation, whereas PARK9 deficiency in astrocytes compromises this protective function. These results highlight astrocyte-mediated a-synuclein clearance as a potential therapeutic target in disorders characterized by the accumulation of a-synuclein including Parkinson’s disease (Tsunemi at al, J. Neurosci. 2019 and 2020).
Effective start/end date9/30/208/31/21


  • National Institute of Neurological Disorders and Stroke (4R37NS096241-05)


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