The DOI matches its Crossref record; 10 of the 10 references it cites were found in a registry or an index.
Impairment of microtubule‐dependent trafficking by overexpression of α‐synuclein
Abstract
Abnormal accumulation of α‐synuclein (α‐syn) has been linked to several neurological disorders, including Parkinson's disease (PD). However, the underlying mechanism by which α‐syn accumulation affects neuronal function and survival remains unknown. Here, we provide data suggesting a possible effect of aggregated α‐syn on the microtubule (MT) network. Consistent with the MT dysfunction, we also observed other degenerative changes, such as neuritic degeneration, trafficking defects, and Golgi fragmentation, which are common pathological features shared by many human neurodegenerative diseases. Neuritic degeneration and Golgi fragmentation were confirmed in primary cultures of dorsal root ganglia (DRG) neurons overexpressing α‐syn. This effect of α‐syn seems to have some selectivity to the MT system, as actin microfilaments and MT‐independent trafficking remain unaffected. Within the degenerating neurites, we found numerous spherical co‐aggregates of α‐syn and tubulins, from which actin was excluded. These studies suggest that the MT system is a potential target of α‐syn, and impairment of this system might have impacts on neuronal structure and function.
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Citations
Cites
AlaSOPro mutation in the gene encoding α-synuclein in Parkinson's disease
Krüger, R., Kuhn, W., Müller, T., Woitalla, D., Graeber, M., Kösel, S., Przuntek, H., Epplen, J. T., Schols, L., & Riess, O. (1998) · Nature Genetics · doi:10.1038/ng0298-106 · Cited by 3,836
Association of missense and 5′-splice-site mutations in tau with the inherited dementia FTDP-17
Hutton, M., Lendon, C. L., Rizzu, P., Baker, M., Froelich, S., Houlden, H., Pickering-Brown, S., Chakraverty, S., Isaacs, A., Grover, A., et al. (1998) · Nature · doi:10.1038/31508 · Cited by 3,498
α-synuclein locus duplication as a cause of familial Parkinson's disease
Chartier-Harlin, M.-C., Kachergus, J., Roumier, C., Mouroux, V., Douay, X., Lincoln, S., Levecque, C., Larvor, L., Andrieux, J., Hulihan, M., et al. (2004) · The Lancet · doi:10.1016/s0140-6736(04)17103-1 · Cited by 2,029
Impaired Degradation of Mutant α-Synuclein by Chaperone-Mediated Autophagy
Cuervo, A. M., Stefanis, L., Fredenburg, R., Lansbury, P. T., & Sulzer, D. (2004) · Science · doi:10.1126/science.1101738 · Cited by 2,024 · cited 2×
“Some of these have yet to be tested in cells (Volles et al., 2001; Cuervo et al., 2004), and others were only found with PD-linked mutants (Stefanis et al., 2001; Tanaka et al., 2001; Cuervo et al., 2004).”
BackgroundMice Lacking α-Synuclein Display Functional Deficits in the Nigrostriatal Dopamine System
Abeliovich, A., Schmitz, Y., Fariñas, I., Choi-Lundberg, D., Ho, W.-H., Castillo, P. E., Shinsky, N., Verdugo, J. M. G., Armanini, M., Ryan, A., et al. (2000) · Neuron · doi:10.1016/s0896-6273(00)80886-7 · Cited by 1,722
Initiation and Synergistic Fibrillization of Tau and Alpha-Synuclein
Giasson, B. I., Forman, M. S., Higuchi, M., Golbe, L. I., Graves, C. L., Kotzbauer, P. T., Trojanowski, J. Q., & Lee, V. M.-Y. (2003) · Science · doi:10.1126/science.1082324 · Cited by 879 · cited 1×
“Journal Compilation ª Federation of European Neuroscience Societies and Blackwell Publishing Ltd European Journal of Neuroscience, 24, 3153–3162 and in vivo (Giasson et al., 2003).”
BackgroundClearance of α-Synuclein Oligomeric Intermediates via the Lysosomal Degradation Pathway
Lee, H.-J., Khoshaghideh, F., Patel, S., & Lee, S.-J. (2004) · The Journal of Neuroscience · doi:10.1523/jneurosci.3809-03.2004 · Cited by 445
Self-citationJensen, P. H., Hager, H., Nielsen, M. S., Højrup, P., Gliemann, J., & Jakes, R. (1999) · Journal of Biological Chemistry · doi:10.1074/jbc.274.36.25481 · Cited by 377
Cooper, J. D., Salehi, A., Delcroix, J.-D., Howe, C. L., Belichenko, P. V., Chua-Couzens, J., Kilbridge, J. F., Carlson, E. J., Epstein, C. J., & Mobley, W. C. (2001) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.181219298 · Cited by 336
α‐Synuclein produces a long‐lasting increase in neurotransmitter release
Liu, S., Ninan, I., Antonova, I., Battaglia, F., Trinchese, F., Narasanna, A., Kolodilov, N., Dauer, W., Hawkins, R. D., & Arancio, O. (2004) · The EMBO Journal · doi:10.1038/sj.emboj.7600451 · Cited by 198
Cited by
-Synuclein in Parkinson's Disease
Stefanis, L. (2012) · Cold Spring Harbor Perspectives in Medicine · doi:10.1101/cshperspect.a009399 · Cited by 1,446
Bendor, J. T., Logan, T. P., & Edwards, R. H. (2013) · Neuron · doi:10.1016/j.neuron.2013.09.004 · Cited by 825
Cell Biology and Pathophysiology of α-Synuclein
Burré, J., Sharma, M., & Südhof, T. C. (2018) · Cold Spring Harbor Perspectives in Medicine · doi:10.1101/cshperspect.a024091 · Cited by 579
Mitochondria: The Next (Neurode)Generation
Schon, E. A., & Przedborski, S. (2011) · Neuron · doi:10.1016/j.neuron.2011.06.003 · Cited by 568
Pathological roles of α-synuclein in neurological disorders
Vekrellis, K., Xilouri, M., Emmanouilidou, E., Rideout, H. J., & Stefanis, L. (2011) · The Lancet Neurology · doi:10.1016/s1474-4422(11)70213-7 · Cited by 357
Metadata
- Authors
- Lee, H., Khoshaghideh, F., Lee, S., & Lee, S.
- Venue
- European Journal of Neuroscience
- Publisher
- Wiley
- Published
- 2006-12
- Volume
- 24
- Issue
- 11
- Pages
- 3153-3162
- ISSN
- 0953-816X (ISSN-L)
- 1460-9568
- OpenAlex
- W2160442779
- Cited by
- 158
- References
- 10
- FWCI
- 5.02
- Type
- journal article
- Language
- en
- Open access
- closed
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