The DOI matches its Crossref record; 11 of the 11 references it cites were found in a registry or an index.
Absence of nigral degeneration in aged parkin/DJ‐1/PINK1 triple knockout mice
Open accessAbstract
Recessively inherited loss‐of‐function mutations in the parkin, DJ‐1, or PINK1 gene are linked to familial cases of early‐onset Parkinson’s diseases (PD), and heterozygous mutations are associated with increased incidence of late‐onset PD. We previously reported that single knockout mice lacking Parkin, DJ‐1, or PINK1 exhibited no nigral degeneration, even though evoked dopamine release from nigrostriatal terminals was reduced and striatal synaptic plasticity was impaired. In this study, we tested whether inactivation of all three recessive PD genes, each of which was required for nigral neuron survival in the aging human brain, resulted in nigral degeneration during the lifespan of mice. Surprisingly, we found that triple knockout mice lacking Parkin, DJ‐1, and PINK1 have normal morphology and numbers of dopaminergic and noradrenergic neurons in the substantia nigra and locus coeruleus, respectively, at the ages of 3, 16, and 24 months. Interestingly, levels of striatal dopamine in triple knockout mice were normal at 16 months of age but increased at 24 months. These results demonstrate that inactivation of all three recessive PD genes is insufficient to cause significant nigral degeneration within the lifespan of mice, suggesting that these genes may be protective rather than essential for the survival of dopaminergic neurons during the aging process. These findings also support the notion that mammalian Parkin and PINK1 may function in the same genetic pathway as in Drosophila.
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Cites
Hereditary Early-Onset Parkinson's Disease Caused by Mutations in PINK1
Valente, E. M., Abou-Sleiman, P. M., Caputo, V., Muqit, M. M. K., Harvey, K., Gispert, S., Ali, Z., Del Turco, D., Bentivoglio, A. R., Healy, D. G., et al. (2004) · Science · doi:10.1126/science.1096284 · Cited by 3,481
Drosophila pink1 is required for mitochondrial function and interacts genetically with parkin
Clark, I. E., Dodson, M. W., Jiang, C., Cao, J. H., Huh, J. R., Seol, J. H., Yoo, S. J., Hay, B. A., & Guo, M. (2006) · Nature · doi:10.1038/nature04779 · Cited by 1,788
Mitochondrial dysfunction in Drosophila PINK1 mutants is complemented by parkin
Park, J., Lee, S. B., Lee, S., Kim, Y., Song, S., Kim, S., Bae, E., Kim, J., Shong, M., Kim, J.-M., et al. (2006) · Nature · doi:10.1038/nature04788 · Cited by 1,705
Mitochondrial pathology and apoptotic muscle degeneration in Drosophila parkin mutants
Greene, J. C., Whitworth, A. J., Kuo, I., Andrews, L. A., Feany, M. B., & Pallanck, L. J. (2003) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0737556100 · Cited by 1,203
Parkin-deficient Mice Exhibit Nigrostriatal Deficits but Not Loss of Dopaminergic Neurons
Goldberg, M. S., Fleming, S. M., Palacino, J. J., Cepeda, C., Lam, H. A., Bhatnagar, A., Meloni, E. G., Wu, N., Ackerson, L. C., Klapstein, G. J., et al. (2003) · Journal of Biological Chemistry · doi:10.1074/jbc.m308947200 · Cited by 913
Self-citationYang, Y., Gehrke, S., Imai, Y., Huang, Z., Ouyang, Y., Wang, J.-W., Yang, L., Beal, M. F., Vogel, H., & Lu, B. (2006) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0602493103 · Cited by 798
Loss of PINK1 causes mitochondrial functional defects and increased sensitivity to oxidative stress
Gautier, C. A., Kitada, T., & Shen, J. (2008) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0802076105 · Cited by 698
Self-citationParkin-deficient mice are not a robust model of parkinsonism
Perez, F. A., & Palmiter, R. D. (2005) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0409598102 · Cited by 477
Mitochondrial localization of DJ‐1 leads to enhanced neuroprotection
Junn, E., Jang, W. H., Zhao, X., Jeong, B. S., & Mouradian, M. M. (2009) · Journal of Neuroscience Research · doi:10.1002/jnr.21831 · Cited by 320
PINK1 is necessary for long term survival and mitochondrial function in human dopaminergic neurons
Wood-Kaczmar, A., Gandhi, S., Yao, Z., Abramov, A. S. Y., Miljan, E. A., Keen, G., Stanyer, L., Hargreaves, I., Klupsch, K., Deas, E., et al. (2008) · PLoS ONE · doi:10.1371/journal.pone.0002455 · Cited by 316
Cited by
The Roles of PINK1, Parkin, and Mitochondrial Fidelity in Parkinson’s Disease
Pickrell, A. M., & Youle, R. J. (2015) · Neuron · doi:10.1016/j.neuron.2014.12.007 · Cited by 2,310
A new pathway for mitochondrial quality control: Mitochondrial-derived vesicles
Sugiura, A., McLelland, G., Fon, E. A., & McBride, H. M. (2014) · The EMBO Journal · doi:10.15252/embj.201488104 · Cited by 862
Parkinson’s disease: genetics and pathogenesis
Shulman, J. M., De Jager, P. L., & Feany, M. B. (2011) · Annual Review of Pathology: Mechanisms of Disease · doi:10.1146/annurev-pathol-011110-130242 · Cited by 801
Missing pieces in the Parkinson's disease puzzle
Obeso, J. A., Rodriguez-Oroz, M. C., Goetz, C. G., Marin, C., Kordower, J. H., Rodriguez, M., Hirsch, E. C., Farrer, M., Schapira, A. H. V., & Halliday, G. (2010) · Nature Medicine · doi:10.1038/nm.2165 · Cited by 734
Animal models of neurodegenerative diseases
Dawson, T. M., Golde, T. E., & Lagier-Tourenne, C. (2018) · Nature Neuroscience · doi:10.1038/s41593-018-0236-8 · Cited by 576
Metadata
- Authors
- Kitada, T., Tong, Y., Gautier, C. A., & Shen, J.
- Venue
- Journal of Neurochemistry
- Publisher
- Wiley
- Published
- 2009-10-12
- Volume
- 111
- Issue
- 3
- Pages
- 696-702
- ISSN
- 0022-3042 (ISSN-L)
- 1471-4159
- OpenAlex
- W1981727895
- Cited by
- 261
- References
- 11
- FWCI
- 12.00
- Type
- journal article
- Language
- en
- Open access
- green
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- Kitada, T., Tong, Y., Gautier, C. A., & Shen, J. (2009). Absence of nigral degeneration in aged parkin/DJ‐1/PINK1 triple knockout mice. Journal of Neurochemistry. https://doi.org/10.1111/j.1471-4159.2009.06350.x
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