The DOI matches its Crossref record; 45 of the 45 references it cites were found in a registry or an index.
Parkin-deficient mice are not a robust model of parkinsonism
Open accessAbstract
Mutations in the human parkin gene cause autosomal recessive juvenile parkinsonism, a heritable form of Parkinson's disease (PD). To determine whether mutations in the mouse parkin gene ( Park2 ) also result in a parkinsonian phenotype, we generated mice with a targeted deletion of parkin exon 2. Using an extensive behavioral screen, we evaluated neurological function, motor ability, emotionality, learning, and memory in aged Parkin-deficient mice. The behavioral profile of Parkin-deficient mice on a B6;129S4 genetic background was strikingly similar to that of control mice, and most differences were not reproducible by using coisogenic mice on a 129S4 genetic background. Moreover, catecholamine levels in the striatum, olfactory bulb, and spinal cord of Parkin-deficient mice were normal. In contrast to previous studies using independently generated Parkin-deficient mice, we found no evidence for nigrostriatal, cognitive, or noradrenergic dysfunction. Understanding why Parkin-deficient mice do not exhibit robust signs of parkinsonism could advance knowledge and treatment of PD.
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“Importantly, parkin-deficient mice and mice expressing a dominant negative form of Nrdp1 are not reported to have significant neurodegenerative disease171819.”
From Clec16a is Critical for Autolysosome Function and Purkinje Cell Survival (2016) · cites this paper as [17]
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“The lack of reported neurodegeneration in parkin-deficient and Nrdp1 mutant mice171819 makes it unlikely that this interaction explains our finding of neurodegeneration in Clec16a mutant mice.”
From Clec16a is Critical for Autolysosome Function and Purkinje Cell Survival (2016) · cites this paper as [17]
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Metadata
- Authors
- Perez, F. A., & Palmiter, R. D.
- Affiliations
- Howard Hughes Medical Institute (US)
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 2005-01-31
- Volume
- 102
- Issue
- 6
- Pages
- 2174-2179
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- PMC
- PMC548311
- OpenAlex
- W2129698492
- Cited by
- 477
- References
- 45
- Citations by year
- 2026: 6 · 2025: 9 · 2024: 18 · 2023: 18 · 2022: 31 · 2021: 33 · 2020: 29 · 2019: 18 · 2018: 24 · 2017: 18 · 2016: 19 · 2015: 17 · 2014: 26 · 2013: 21 · 2012: 27
- FWCI
- 19.69
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Locations
- Proceedings of the National Academy of Sciences (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Clinical Neurology › Parkinson's Disease Mechanisms and Treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nuclear Receptors and Signaling
- Health Sciences › Medicine › Clinical Neurology › Deep Brain Stimulation and Movement Disorders
- Keywords
- Parkin, PARK2, juvenile parkinsonism, autosomal recessive juvenile parkinsonism, Parkinson's disease, exon 2 deletion, behavioral phenotypes, motor function, emotionality, learning and memory, catecholamine levels, noradrenergic dysfunction, genetic background effects, B6
- MeSH terms
- Amphetamines, Animals, Behavior, Animal, Disease Models, Animal, Emotions, Genotype, Humans, Learning, Memory, Mice, Inbred C57BL, Motor Activity, Nerve Tissue, Parkinson Disease, Phenotype, Mice, Knockout, Ubiquitin-Protein Ligases, Mice
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