The DOI matches its Crossref record; 7 of the 7 references it cites were found in a registry or an index.
Formation of α-synuclein Lewy neurite–like aggregates in axons impedes the transport of distinct endosomes
Open accessAbstract
Aggregates of α-synuclein (α-syn) accumulate in neurons in Parkinson's disease and other synucleinopathies. These inclusions predominantly localize to axons even in the early stages of the disease, but their affect on axon function has remained unknown. Previously we established a model in which the addition of preformed α-syn fibrils to primary neurons seeds formation of insoluble α-syn inclusions built from endogenously expressed α-syn that closely recapitulate the neuropathological phenotypes of Lewy neurites found in human diseased brains. Here we show, using live-cell imaging, that immobile α-syn inclusions accumulate in axons from the recruitment of α-syn located on mobile α-syn–positive vesicles. Ultrastructural analyses and live imaging demonstrate that α-syn accumulations do not cause a generalized defect in axonal transport; the inclusions do not fill the axonal cytoplasm, disrupt the microtubule cytoskeleton, or affect the transport of synaptophysin or mitochondria. However, the α-syn aggregates impair the transport of Rab7 and TrkB receptor–containing endosomes, as well as autophagosomes. In addition, the TrkB receptor–associated signaling molecule pERK5 accumulates in α-syn aggregate–bearing neurons. Thus α-syn pathology impairs axonal transport of signaling and degradative organelles. These early effects of α-syn accumulations may predict points of intervention in the neurodegenerative process.
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Cites
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Autophagosomes initiate distally and mature during transport toward the cell soma in primary neurons
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Distinct α-Synuclein Strains Differentially Promote Tau Inclusions in Neurons
Guo, J. L., Covell, D. J., Daniels, J. P., Iba, M., Stieber, A., Zhang, B., Riddle, D. M., Kwong, L. K., Xu, Y., Trojanowski, J. Q., et al. (2013) · Cell · doi:10.1016/j.cell.2013.05.057 · Cited by 680
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Double-knockout mice for α- and β-synucleins: Effect on synaptic functions
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Lewy Body-like α-Synuclein Aggregates Resist Degradation and Impair Macroautophagy
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Calabresi, P., Mechelli, A., Natale, G., Volpicelli-Daley, L., Di Lazzaro, G., & Ghiglieri, V. (2023) · Cell Death & Disease · doi:10.1038/s41419-023-05672-9 · Cited by 817
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Metadata
- Authors
- Volpicelli-Daley, L. A., Gamble, K. L., Schultheiss, C. E., Riddle, D. M., West, A. B., & Lee, V. M.-Y.
- Venue
- Molecular Biology of the Cell
- Published
- 2014-12-15
- Volume
- 25
- Issue
- 25
- Pages
- 4010-4023
- ISSN
- 1059-1524 (ISSN-L)
- 1939-4586
- OpenAlex
- W2325022883
- Cited by
- 232
- References
- 7
- FWCI
- 10.28
- Type
- journal article
- Language
- en
- Open access
- green
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- The paper
- Volpicelli-Daley, L. A., Gamble, K. L., Schultheiss, C. E., Riddle, D. M., West, A. B., & Lee, V. M.-Y. (2014). Formation of α-synuclein Lewy neurite–like aggregates in axons impedes the transport of distinct endosomes. Molecular Biology of the Cell. https://doi.org/10.1091/mbc.e14-02-0741
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