The DOI matches its Crossref record; 5 of the 5 references it cites were found in a registry or an index.
Mutant huntingtin aggregates impair mitochondrial movement and trafficking in cortical neurons
Open accessAbstract
Huntington's disease (HD) is a neurodegenerative disorder caused by a polyglutamine repeat in the huntingtin gene (Htt). Mitochondrial defects and protein aggregates are characteristic of affected neurons. Recent studies suggest that these aggregates impair cellular transport mechanisms by interacting with cytoskeletal components and molecular motors. Here, we investigated whether mutant Htt alters mitochondrial trafficking and morphology in primary cortical neurons. We demonstrate that full-length mutant Htt was more effective than N-terminal mutant Htt in blocking mitochondrial movement, an effect that correlated with its heightened expression in the cytosolic compartment. Aggregates impaired the passage of mitochondria along neuronal processes, causing mitochondria to accumulate adjacent to aggregates and become immobilized. Furthermore, mitochondrial trafficking was reduced specifically at sites of aggregates while remaining unaltered in regions lacking aggregates. We conclude that in cortical neurons, an early event in HD pathophysiology is the aberrant mobility and trafficking of mitochondria caused by cytosolic Htt aggregates.
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Cites
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Early mitochondrial calcium defects in Huntington's disease are a direct effect of polyglutamines
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Mutant huntingtin impairs axonal trafficking in mammalian neurons in vivo and in vitro
Trushina, E., Dyer, R. B., Badger, J. D., Ure, D., Eide, L., Tran, D. D., Vrieze, B. T., Legendre-Guillemin, V., McPherson, P. S., Mandavilli, B. S., et al. (2004) · Molecular and Cellular Biology · doi:10.1128/mcb.24.18.8195-8209.2004 · Cited by 520
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Mattson, M. P., Gleichmann, M., & Cheng, A. (2008) · Neuron · doi:10.1016/j.neuron.2008.10.010 · Cited by 1,081
Molecular Mechanisms and Potential Therapeutical Targets in Huntington's Disease
Zuccato, C., Valenza, M., & Cattaneo, E. (2010) · Physiological Reviews · doi:10.1152/physrev.00041.2009 · Cited by 848
Mitochondria: The Next (Neurode)Generation
Schon, E. A., & Przedborski, S. (2011) · Neuron · doi:10.1016/j.neuron.2011.06.003 · Cited by 568
Mitochondria and Reactive Oxygen Species in Aging and Age-Related Diseases
(2018) · International Review of Cell and Molecular Biology · doi:10.1016/bs.ircmb.2018.05.006 · Cited by 455
Huntington's disease: from pathology and genetics to potential therapies
Imarisio, S., Carmichael, J., Korolchuk, V., Chen, C.-W., Saiki, S., Rose, C., Krishna, G., Davies, J. E., Ttofi, E., Underwood, B. R., et al. (2008) · Biochemical Journal · doi:10.1042/bj20071619 · Cited by 409
Metadata
- Authors
- Chang, D. T. W., Rintoul, G. L., Pandipati, S., & Reynolds, I. J.
- Venue
- Neurobiology of Disease
- Publisher
- Elsevier BV
- Published
- 2006-05
- Volume
- 22
- Issue
- 2
- Pages
- 388-400
- ISSN
- 0969-9961 (ISSN-L)
- OpenAlex
- W2016888445
- Cited by
- 299
- References
- 5
- FWCI
- 6.36
- Type
- journal article
- Language
- en
- Open access
- green
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