The DOI matches its Crossref record; 23 of the 23 references it cites were found in a registry or an index.
Development and Characterization of a New Parkinson's Disease Model Resulting from Impaired Autophagy
Open accessAbstract
Parkinson's disease (PD) is a progressive neurodegenerative disease caused by the interaction of genetic and environmental factors. However, the etiology of PD remains largely unknown. Macroautophagy is known to play an essential role in the degradation of abnormal proteins and organelles. Furthermore, the loss of autophagy-related (Atg) genes results in neurodegeneration and abnormal protein accumulation. Since these are also pathologic features of Parkinson's disease, the conditional impairment of autophagy may lead to improved animal models for the study of PD. Using transgenic mice expressing Cre recombinase under the control of either the dopamine transporter or the engrailed-1 promoters, we generated mice with the conditional deletion of Atg7 in the dopamine neurons of the substantia nigra pars compacta, other regions of the midbrain, and also the hindbrain. This conditional impairment of autophagy results in the age-related loss of dopaminergic neurons and corresponding loss of striatal dopamine, the accumulation of low-molecular-weight α-synuclein, and the presence of ubiquitinated protein aggregates, recapitulating many of the pathologic features of PD. These conditional knock-out animals provide insight into the process of autophagy in Parkinson's disease pathology.
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“Several lines of evidence indicate a role for autophagy in the regulation of synuclein homeostasis5,6,15, suggesting that dysfunctional autophagic clearance may contribute to the development of synuclein inclusions.”
From Loss of autophagy in dopaminergic neurons causes Lewy pathology and motor dysfunction in aged mice (2018) · cites this paper as [15]
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Metadata
- Authors
- Ahmed, I., Liang, Y., Schools, S., Dawson, V. L., Dawson, T. M., & Savitt, J. M.
- Affiliations
- Johns Hopkins University (US)
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2012-11-14
- Volume
- 32
- Issue
- 46
- Pages
- 16503-16509
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- PMC
- PMC3508432
- OpenAlex
- W2026969412
- Cited by
- 144
- References
- 23
- Citations by year
- 2026: 1 · 2025: 6 · 2024: 5 · 2023: 6 · 2022: 10 · 2021: 19 · 2020: 10 · 2019: 13 · 2018: 10 · 2017: 8 · 2016: 16 · 2015: 12 · 2014: 16 · 2013: 12
- FWCI
- 8.36
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Neuroscience (publishedVersion, cc-by-nc-sa)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- Funders
- Parkinson's Disease Foundation
- Adrienne Helis Malvin Medical Research Foundation
- JPB Foundation
- Johns Hopkins University
- National Institutes of Health
- National Institute of Neurological Disorders and Stroke (P50NS38377, K08NS052624, P50NS038377)
- Topics
- Health Sciences › Medicine › Clinical Neurology › Parkinson's Disease Mechanisms and Treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Autophagy in Disease and Therapy
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nuclear Receptors and Signaling
- Keywords
- Parkinson's disease, autophagy, ATG7, conditional knockout mice, dopaminergic neurons, substantia nigra pars compacta, alpha-synuclein aggregation, ubiquitinated protein aggregates, striatal dopamine, neurodegeneration, transgenic mice
- MeSH terms
- Autophagy-Related Protein 7, Dynactin Complex, Animals, Autophagy, Cell Count, Chromatography, High Pressure Liquid, Disease Models, Animal, Dopamine, Electrochemistry, Immunohistochemistry, Microtubule-Associated Proteins, Parkinson Disease, Blotting, Western, Neostriatum, Gene Deletion, Mice, Knockout, Neurotransmitter Agents, Ubiquitin, Polyubiquitin, Mice, alpha-Synuclein, Dopaminergic Neurons
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