The DOI matches its Crossref record; 15 of the 15 references it cites were found in a registry or an index.
Mono- and double-mutant mouse models of Parkinson's disease display severe mitochondrial damage
Open accessAbstract
Mutations in the gene encoding alpha-synuclein (asyn) causes autosomal-dominant, in the parkin gene autosomal-recessive forms of Parkinson's disease (PD). The pathophysiology of PD is poorly understood, even though published evidence suggests a role for mitochondria in the pathogenesis. To gain insight into the influence of asyn and parkin on mitochondrial integrity and function, we have generated several mono-mutant mouse lines expressing doubly mutated human asyn (hm(2)asyn) under the control of two different promoters, or a targeted deletion of Parkin (Parkin-Exon3-knockout). Both mouse lines were crossed to generate the double-mutant. Here we compare the ultrastructure and functional properties of mitochondria in the substantia nigra (SN), the striatum, the cerebral cortex (Cx) and skeletal muscle of young (2-3 months) and aged (12-14 months) mono- and double-mutants mice. We observed severe genotype-, age- and region-dependent morphological alterations of mitochondria in neuronal somata. The number of structurally altered mitochondria was significantly increased in the SN of both double-mutants and in the Cx of one mono- and one double-mutant line. These alterations coincided with a reduced complex I capacity in the SN, but were neither accompanied by alterations in the number or the size of the mitochondria nor by leakage of cytochrome c, Smac/DIABLO or Omi/HtrA2. None of the transgenic animals developed any gross histopathological abnormalities or overt motor disabilities. Together our results provide compelling evidence that (i) both, asyn and parkin are relevant for mitochondrial integrity, (ii) the influence of these proteins on mitochondria are age- and tissue-specific and (iii) changes of mitochondrial morphology do not inevitably cause functional impairments.
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Cites
Mitochondrial Dysfunction and Oxidative Stress in Neurodegenerative Diseases
Lin, M. T., & Beal, M. F. (2006) · Nature · doi:10.1038/nature05292 · Cited by 6,455
Triple-Transgenic Model of Alzheimer’s Disease with Plaques and Tangles
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Drosophila pink1 is required for mitochondrial function and interacts genetically with parkin
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Mitochondrial dysfunction in Drosophila PINK1 mutants is complemented by parkin
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Parkin-deficient Mice Exhibit Nigrostriatal Deficits but Not Loss of Dopaminergic Neurons
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Expanding insights of mitochondrial dysfunction in Parkinson's disease
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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
The Role of Oxidative Stress in Parkinson's Disease
Dias, V., Junn, E., & Mouradian, M. M. (2013) · Journal of Parkinson’s Disease · doi:10.3233/jpd-130230 · Cited by 1,845
Mitochondria in neuroplasticity and neurological disorders
Mattson, M. P., Gleichmann, M., & Cheng, A. (2008) · Neuron · doi:10.1016/j.neuron.2008.10.010 · Cited by 1,081
Bendor, J. T., Logan, T. P., & Edwards, R. H. (2013) · Neuron · doi:10.1016/j.neuron.2013.09.004 · Cited by 825
Thomas, B., & Beal, M. F. (2007) · Human Molecular Genetics · doi:10.1093/hmg/ddm159 · Cited by 748
Metadata
- Authors
- Stichel, C. C., Zhu, X.-R., Bader, V., Linnartz, B., Schmidt, S., & Lubbert, H.
- Venue
- Human Molecular Genetics
- Publisher
- Oxford University Press (OUP)
- Published
- 2007-04-05
- Volume
- 16
- Issue
- 20
- Pages
- 2377-2393
- ISSN
- 0964-6906 (ISSN-L)
- 1460-2083
- OpenAlex
- W2119489612
- Cited by
- 179
- References
- 15
- FWCI
- 10.65
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Stichel, C. C., Zhu, X.-R., Bader, V., Linnartz, B., Schmidt, S., & Lubbert, H. (2007). Mono- and double-mutant mouse models of Parkinson's disease display severe mitochondrial damage. Human Molecular Genetics. https://doi.org/10.1093/hmg/ddm083
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