Journal
NATURE COMMUNICATIONS
Volume 5, Issue -, Pages -Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/ncomms5755
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Funding
- National Research Foundation (NRF) - Korean Government [2010-0015188]
- Korea Health Technology R&D Project, Ministry of Health & Welfare, Republic of Korea [A111228]
- NIH [AG18440, AG022074]
- Konkuk University
- Korea Health Promotion Institute [A111228] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
- National Research Foundation of Korea [2010-0015188] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
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Deposition of alpha-synuclein aggregates occurs widely in the central and peripheral nervous systems in Parkinson's disease (PD). Although recent evidence has suggested that cell-to-cell transmission of alpha-synuclein aggregates is associated with the progression of PD, the mechanism by which alpha-synuclein aggregates spread remains undefined. Here, we show that alpha-synuclein aggregates are transmitted from cell to cell through a cycle involving uptake of external aggregates, co-aggregation with endogenous alpha-synuclein and exocytosis of the co-aggregates. Moreover, we find that glucocerebrosidase depletion, which has previously been strongly associated with PD and increased cognitive impairment, promotes propagation of alpha-synuclein aggregates. These studies define how alpha-synuclein aggregates spread among neuronal cells and may provide an explanation for how glucocerebrosidase mutations increase the risk of developing PD and other synucleinopathies.
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