Cited by 477Parkinson's Disease Mechanisms and TreatmentsNuclear Receptors and SignalingDeep Brain Stimulation and Movement Disorders

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Parkin-deficient mice are not a robust model of parkinsonism

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Perez, Francisco A., Palmiter, Richard D.·2005·Proceedings of the National Academy of Sciences

DOI 10.1073/pnas.0409598102PMC PMC548311

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Abstract

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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Authors: Perez, F. A., & Palmiter, R. D.
Affiliations: Howard Hughes Medical Institute (US)
ORCID: Perez, Francisco A.
Palmiter, Richard D.
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
DOI: 10.1073/pnas.0409598102
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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Parkin-deficient mice are not a robust model of parkinsonism

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