The DOI matches its Crossref record; 136 of the 136 references it cites were found in a registry or an index.
Modeling Parkinson’s Disease With the Alpha-Synuclein Protein
Open accessAbstract
gene, which encodes α-Syn, cause familial forms of PD and are the basis of sporadic PD risk. Given the role of the α-Syn protein in the pathology of PD, animal models that reflect the dopaminergic neuronal loss and the widespread and progressive formation of α-Syn aggregates in different areas of the brain constitute a valuable tool. Indeed, animal models of PD are important for understanding the molecular mechanisms of the disease and might contribute to the development and validation of new therapies. In the absence of animal models that faithfully reproduce human PD, in recent years, numerous animal models of PD based on α-Syn have been generated. In this review, we summarize the main features of the α-Syn pre-formed fibrils (PFFs) model and recombinant adeno-associated virus vector (rAAV) mediated α-Syn overexpression models, providing a detailed comparative analysis of both models. Here, we discuss how each model has contributed to our understanding of PD pathology and the advantages and weakness of each of them. SIGNIFICANCE: Here, we show that injection of α-Syn PFFs and overexpression of α-Syn mediated by rAAV lead to a different pattern of PD pathology in rodents. First, α-Syn PFFs models trigger the Lewy body-like inclusions formation in brain regions directly interconnected with the injection site, suggesting that there is an inter-neuronal transmission of the α-Syn pathology. In contrast, rAAV-mediated α-Syn overexpression in the brain limits the α-Syn aggregates within the transduced neurons. Second, phosphorylated α-Syn inclusions obtained with rAAV are predominantly nuclear with a punctate appearance that becomes diffuse along the neuronal fibers, whereas α-Syn PFFs models lead to the formation of cytoplasmic aggregates of phosphorylated α-Syn reminiscent of Lewy bodies and Lewy neurites.
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Staging of brain pathology related to sporadic Parkinson’s disease
Braak, H., Tredici, K. D., Rüb, U., de Vos, R. A. I., Jansen Steur, E. N. H., & Braak, E. (2003) · Neurobiology of Aging · doi:10.1016/s0197-4580(02)00065-9 · Cited by 10,777
Spillantini, M. G., Schmidt, M. L., Lee, V. M.-Y., Trojanowski, J. Q., Jakes, R., & Goedert, M. (1997) · Nature · doi:10.1038/42166 · Cited by 8,382
Mutation in the α-Synuclein Gene Identified in Families with Parkinson's Disease
Polymeropoulos, M. H., Lavedan, C., Leroy, E., Ide, S. E., Dehejia, A., Dutra, A., Pike, B., Root, H., Rubenstein, J., Boyer, R., et al. (1997) · Science · doi:10.1126/science.276.5321.2045 · Cited by 8,240
Kalia, L. V., & Lang, A. E. (2015) · The Lancet · doi:10.1016/s0140-6736(14)61393-3 · Cited by 6,184
Dauer, W., & Przedborski, S. (2003) · Neuron · doi:10.1016/s0896-6273(03)00568-3 · Cited by 5,469
The new mutation, E46K, of α‐synuclein causes parkinson and Lewy body dementia
Zarranz, J. J., Alegre, J., Gómez‐Esteban, J. C., Lezcano, E., Ros, R., Ampuero, I., Vidal, L., Hoenicka, J., Rodriguez, O., Atarés, B., et al. (2004) · Annals of Neurology · doi:10.1002/ana.10795 · Cited by 2,737
Stages in the development of Parkinson’s disease-related pathology
Braak, H., Ghebremedhin, E., Rüb, U., Bratzke, H., & Del Tredici, K. (2004) · Cell and Tissue Research · doi:10.1007/s00441-004-0956-9 · Cited by 2,689
Luk, K. C., Kehm, V., Carroll, J., Zhang, B., O’Brien, P., Trojanowski, J. Q., & Lee, V. M.-Y. (2012) · Science · doi:10.1126/science.1227157 · Cited by 2,563
Non-motor features of Parkinson disease
Schapira, A. H. V., Chaudhuri, K. R., & Jenner, P. (2017) · Nature Reviews Neuroscience · doi:10.1038/nrn.2017.62 · Cited by 2,053
International Parkinson's Disease Genomics Consortium (IPDGC), Nalls, M. A., Parkinson's Study Group (PSG) Parkinson's Research: The Organized GENetics Initiative (PROGENI), 23andMe, GenePD, NeuroGenetics Research Consortium (NGRC), Hussman Institute of Human Genomics (HIHG), Investigator, T. A. J. D., (CHARGE), C. F. H. A. A. R. I. G. E., North American Brain Expression Consortium (NABEC), et al. (2014) · Nature Genetics · doi:10.1038/ng.3043 · Cited by 1,895
Cited by
Adamu, A., Li, S., Gao, F., & Xue, G. (2024) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2024.1347987 · Cited by 564
α-Synuclein misfolding and aggregation: Implications in Parkinson’s disease pathogenesis
Mehra, S., Sahay, S., & Maji, S. K. (2019) · Biochimica et Biophysica Acta (BBA) - Proteins and Proteomics · doi:10.1016/j.bbapap.2019.03.001 · Cited by 499
Glucagon-like peptide-1: a multi-faceted anti-inflammatory agent
Mehdi, S. F., Pusapati, S., Anwar, M. S., Lohana, D., Kumar, P., Nandula, S. A., Nawaz, F. K., Tracey, K., Yang, H., LeRoith, D., et al. (2023) · Frontiers in Immunology · doi:10.3389/fimmu.2023.1148209 · Cited by 317
Impaired dopamine release in Parkinson’s disease
Cramb, K. M. L., Beccano-Kelly, D., Cragg, S. J., & Wade-Martins, R. (2023) · Brain · doi:10.1093/brain/awad064 · Cited by 207
Progress and Challenges in Targeted Protein Degradation for Neurodegenerative Disease Therapy
Fang, Y., Wang, J., Zhao, M., Zheng, Q., Ren, C., Wang, Y., & Zhang, J. (2022) · Journal of Medicinal Chemistry · doi:10.1021/acs.jmedchem.2c00844 · Cited by 100
Metadata
- Authors
- Gómez-Benito, M., Granado, N., García-Sanz, P., Michel, A., Dumoulin, M., & Moratalla, R.
- Venue
- Frontiers in Pharmacology
- Publisher
- Frontiers Media SA
- Published
- 2020-04-23
- Volume
- 11
- Pages
- 356-356
- ISSN
- 1663-9812 (ISSN-L)
- OpenAlex
- W3016614566
- Cited by
- 437
- References
- 136
- FWCI
- 18.08
- Type
- journal article
- Language
- en
- Open access
- gold
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