The DOI matches its Crossref record; 14 of the 14 references it cites were found in a registry or an index.
Parkinson Phenotype in Aged PINK1-Deficient Mice Is Accompanied by Progressive Mitochondrial Dysfunction in Absence of Neurodegeneration
Open accessAbstract
BACKGROUND: Parkinson's disease (PD) is an adult-onset movement disorder of largely unknown etiology. We have previously shown that loss-of-function mutations of the mitochondrial protein kinase PINK1 (PTEN induced putative kinase 1) cause the recessive PARK6 variant of PD. METHODOLOGY/PRINCIPAL FINDINGS: Now we generated a PINK1 deficient mouse and observed several novel phenotypes: A progressive reduction of weight and of locomotor activity selectively for spontaneous movements occurred at old age. As in PD, abnormal dopamine levels in the aged nigrostriatal projection accompanied the reduced movements. Possibly in line with the PARK6 syndrome but in contrast to sporadic PD, a reduced lifespan, dysfunction of brainstem and sympathetic nerves, visible aggregates of alpha-synuclein within Lewy bodies or nigrostriatal neurodegeneration were not present in aged PINK1-deficient mice. However, we demonstrate PINK1 mutant mice to exhibit a progressive reduction in mitochondrial preprotein import correlating with defects of core mitochondrial functions like ATP-generation and respiration. In contrast to the strong effect of PINK1 on mitochondrial dynamics in Drosophila melanogaster and in spite of reduced expression of fission factor Mtp18, we show reduced fission and increased aggregation of mitochondria only under stress in PINK1-deficient mouse neurons. CONCLUSION: Thus, aging Pink1(-/-) mice show increasing mitochondrial dysfunction resulting in impaired neural activity similar to PD, in absence of overt neuronal death.
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Citations
Cites
Parkin is recruited selectively to impaired mitochondria and promotes their autophagy
Narendra, D., Tanaka, A., Suen, D.-F., & Youle, R. J. (2008) · The Journal of Cell Biology · doi:10.1083/jcb.200809125 · Cited by 4,026
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
Self-citationDrosophila 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
Bender, A., Krishnan, K. J., Morris, C. M., Taylor, G. A., Reeve, A. K., Perry, R. H., Jaros, E., Hersheson, J. S., Betts, J., Klopstock, T., et al. (2006) · Nature Genetics · doi:10.1038/ng1769 · Cited by 1,570
The PINK1/Parkin pathway regulates mitochondrial morphology
Poole, A. C., Thomas, R. E., Andrews, L. A., McBride, H. M., Whitworth, A. J., & Pallanck, L. J. (2008) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0709336105 · Cited by 885
Rogers, D. C., Fisher, E. M. C., Brown, S. D. M., Peters, J., Hunter, A. J., & Martin, J. E. (1997) · Mammalian Genome · doi:10.1007/s003359900551 · Cited by 795
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
Gandhi, S., Wood-Kaczmar, A., Yao, Z., Plun-Favreau, H., Deas, E., Klupsch, K., Downward, J., Latchman, D. S., Tabrizi, S. J., Wood, N. W., et al. (2009) · Molecular Cell · doi:10.1016/j.molcel.2009.02.013 · Cited by 682
PINK1 Protects against Oxidative Stress by Phosphorylating Mitochondrial Chaperone TRAP1
Pridgeon, J. W., Olzmann, J. A., Chin, L.-S., & Li, L. (2007) · PLoS Biology · doi:10.1371/journal.pbio.0050172 · Cited by 596
Cited by
Gegg, M. E., Cooper, J. M., Chau, K.-Y., Rojo, M., Schapira, A. H. V., & Taanman, J.-W. (2010) · Human Molecular Genetics · doi:10.1093/hmg/ddq419 · Cited by 910
Mitochondrial dysfunction in Parkinson's disease
Winklhofer, K. F., & Haass, C. (2010) · Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease · doi:10.1016/j.bbadis.2009.08.013 · Cited by 688
Murrow, L., & Debnath, J. (2013) · Annual Review of Pathology: Mechanisms of Disease · doi:10.1146/annurev-pathol-020712-163918 · Cited by 527
Schapira, A. H. (2012) · The Lancet · doi:10.1016/s0140-6736(11)61305-6 · Cited by 494
Historical Perspective: Models of Parkinson’s Disease
Chia, S. J., Tan, E.-K., & Chao, Y.-X. (2020) · International Journal of Molecular Sciences · doi:10.3390/ijms21072464 · Cited by 401
Metadata
- Authors
- Gispert, S., Ricciardi, F., Kurz, A., Azizov, M., Hoepken, H.-H., Becker, D., Voos, W., Leuner, K., Müller, W. E., Kudin, A. P., Kunz, W. S., Zimmermann, A., Roeper, J., Wenzel, D., Jendrach, M., García-Arencíbia, M., Fernández-Ruiz, J., Huber, L., Rohrer, H., Barrera, M., Reichert, A. S., Rüb, U., Chen, A., Nussbaum, R. L., & Auburger, G.
- Venue
- PLoS ONE
- Publisher
- Public Library of Science (PLoS)
- Published
- 2009-06-03
- Volume
- 4
- Issue
- 6
- Pages
- e5777
- ISSN
- 1932-6203 (ISSN-L)
- OpenAlex
- W2152817972
- Cited by
- 381
- References
- 14
- FWCI
- 18.19
- Type
- journal article
- Language
- en
- Open access
- gold
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- The paper
- Gispert, S., Ricciardi, F., Kurz, A., Azizov, M., Hoepken, H.-H., Becker, D., Voos, W., Leuner, K., Müller, W. E., Kudin, A. P., Kunz, W. S., Zimmermann, A., Roeper, J., Wenzel, D., Jendrach, M., García-Arencíbia, M., Fernández-Ruiz, J., Huber, L., Rohrer, H., . . . Auburger, G. (2009). Parkinson Phenotype in Aged PINK1-Deficient Mice Is Accompanied by Progressive Mitochondrial Dysfunction in Absence of Neurodegeneration. PLoS ONE. https://doi.org/10.1371/journal.pone.0005777
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
