ArticleBMC neuroscience2017
Early start of progressive motor deficits in Line 61 α-synuclein transgenic mice.
Article in BMC neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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37 citing papers in PubMed, 57 citations in OpenAlex.
- Single-molecule detection methods to study alpha-synuclein aggregation in postmortem Parkinson's disease brains.Cell reports methods · 2026Article
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- Protein phosphatase 2A methylation state impacts α-synucleinopathy in mouse models.Cell death discovery · 2026Article
- Pharmacological inhibition of O-GlcNAcase reduces pS129-α-synuclein positive aggregates in the substantia nigra of mThy1-hSNCA mice.Journal of Parkinson's disease · 2026Article
- Olfactory sensory map is perturbed in a human wild-type α-synuclein overexpressing transgenic mouse model of Parkinson's disease.NPJ Parkinson's disease · 2026Article
- Montelukast alleviates neuroinflammation and improves motor functions in the line 61 model of Parkinson's disease: An exploratory study.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Article
- Synaptic vesicle-omics in mice captures signatures of aging and synucleinopathy.Nature communications · 2025Article
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- Deciphering motor dysfunction and microglial activation in mThy1-Frontiers in molecular neuroscience · 2025Article
- Quantitative systems pharmacology model of α-synuclein pathology in Parkinson's disease-like mouse for investigation of passive immunotherapy mechanisms.CPT: pharmacometrics & systems pharmacology · 2024Article
- Limitations and potential strategies of immune checkpoint blockade in age-related neurodegenerative disorders.The journal of physiological sciences : JPS · 2024Review
- Immunotherapy with an antibody against CD1d modulates neuroinflammation in an α-synuclein transgenic model of Lewy body like disease.Journal of neuroinflammation · 2024Article
- Motor deficits and brain pathology in the Parkinson's disease mouse model hA53Ttg.Frontiers in neuroscience · 2024Article
- Impaired aldehyde detoxification exacerbates motor deficits in an alpha-synuclein mouse model of Parkinson's disease.Brain and behavior · 2023Article
- In vivo effects of the alpha-synuclein misfolding inhibitor minzasolmin supports clinical development in Parkinson's disease.NPJ Parkinson's disease · 2023Article
- A Mouse Model to Test Novel Therapeutics for Parkinson's Disease: an Update on the Thy1-aSyn ("line 61") Mice.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023Review
- How Well Do Rodent Models of Parkinson's Disease Recapitulate Early Non-Motor Phenotypes? A Systematic Review.Biomedicines · 2022Review
- Article
- Modeling Parkinson's disease-related symptoms in alpha-synuclein overexpressing mice.Brain and behavior · 2022Review
- A Novel NOX Inhibitor Treatment Attenuates Parkinson's Disease-Related Pathology in Mouse Models.International journal of molecular sciences · 2022Article
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSynucleinopathies such as Parkinson's disease or multiple system atrophy are characterized by Lewy bodies in distinct brain areas. These aggregates are mainly formed by α-synuclein inclusions, a protein crucial for synaptic functions in the healthy brain. Transgenic animal models of synucleinopathies are frequently based on over-expression of human wild type or mutated α-synuclein under the regulatory control of different promoters. A promising model is the Line 61 α-synuclein transgenic mouse that expresses the transgene under control of the Thy-1 promoter.
resultsHere, we show an extended characterization of this mouse model over age. To this end, we analyzed animals for the progression of human and mouse protein expression levels in different brain areas as well as motor and memory deficits. Our results show, that Line 61 mice exhibited an age dependent increase of α-synuclein protein levels in the hippocampus but not the striatum. While murine α-synuclein was also increased with age, it was lower expressed in Line 61 mice than in non-transgenic littermates. At the age of 9 months animals exhibited increased neuroinflammation. Furthermore, we found that Line 61 mice showed severe motor deficits as early as 1 month of age as assessed by the wire hanging and nest building tests. At later ages, initial motor deficits were validated with the RotaRod, pasta gnawing and beam walk tests. At 8 months of age animals exhibited emotional memory deficits as validated with the contextual fear conditioning test.
conclusionIn summary, our results strengthen and further expand our knowledge about the Line 61 mouse model, emphasizing this mouse model as a valuable in vivo tool to test new compounds directed against synucleinopathies.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.