ReviewNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics2023
A Mouse Model to Test Novel Therapeutics for Parkinson's Disease: an Update on the Thy1-aSyn ("line 61") Mice.
Review in Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics, 2023. 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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Who cites it
37 citing papers in PubMed.
- Rodent models and accompanying in vitro strategies for studying the etiology and therapy of Parkinson's disease.Journal of Parkinson's disease · 2026Review
- Altered light-dark phase-dependent behavioral responses and suprachiasmatic nucleus pathology in an α-synuclein rat model of Parkinson's disease.NPJ Parkinson's disease · 2026Article
- Single-molecule detection methods to study alpha-synuclein aggregation in postmortem Parkinson's disease brains.Cell reports methods · 2026Article
- Potential glutamatergic and GABAergic false neurotransmitters in models of excitation-inhibition imbalance.Scientific reports · 2026Article
- Mouse model of atypical DAT deficiency syndrome uncovers dopamine dysfunction associated with parkinsonism and ADHD.The Journal of clinical investigation · 2026Article
- Faecalibacterium prausnitzii, depleted in the Parkinson's disease microbiome, improves motor deficits in α-synuclein overexpressing mice.NPJ 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
- Comparative Analysis of T-Cell Signatures and Astroglial Reactivity in Parkinson's Pathology Across Animal Models with Distinct Regenerative Capacities.International journal of molecular sciences · 2026Article
- Imaging spatial transcriptomics reveals molecular patterns underlying accumulation of p-Ser129 α-synuclein in a transgenic mouse model.NPJ Parkinson's disease · 2026Article
- Inhibition of TGF-beta signaling protects from alpha-synuclein induced toxicity.Cell death discovery · 2025Article
- Depending on intensity, exercise improved or worsened pathology in a model of prodromal Parkinson's disease.NPJ Parkinson's disease · 2025Article
- Redirecting microglia phenotype via inhibition of NFAT1 ameliorates deficits in mouse model of synucleinopathies.Experimental & molecular medicine · 2025Article
- Nose-to-brain siRNA delivery by PEI/PPI-based nanoparticles reduces α-synuclein expression in a Parkinson's disease mouse model.Molecular therapy. Nucleic acids · 2025Article
- 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
- Recombinant cathepsins B and L promote α-synuclein clearance and restore lysosomal function in human and murine models with α-synuclein pathology.Molecular neurodegeneration · 2025Article
- Early synaptic changes and reduced brain connectivity in PD-like mice with depressive phenotype.NPJ Parkinson's disease · 2025Article
- A genome-wide RNA interference screening reveals protectiveness of SNX5 knockdown in a Parkinson's disease cell model.Translational neurodegeneration · 2025Article
- IGF2-Reprogrammed Macrophages Ameliorate the Inflammatory Response and Protect Against the Neuroinflammatory Process in Parkinson's Disease Models.Aging cell · 2025Article
- Application of IVDr NMR spectroscopy to stratify Parkinson's disease with absolute quantitation of blood serum metabolites and lipoproteins.Scientific reports · 2025Article
- Nose-to-brain drug delivery: from bench to bedside.Translational neurodegeneration · 2025Review
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5 authors.
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Abstract
Development of neuroprotective therapeutics for Parkinson's disease (PD) is facing a lack of translation from pre-clinical to clinical trials. One strategy for improvement is to increase predictive validity of pre-clinical studies by using extensively characterized animal models with a comprehensive set of validated pharmacodynamic readouts. Mice over-expressing full-length, human, wild-type alpha-synuclein under the Thy-1 promoter (Thy1-aSyn line 61) reproduce key features of sporadic PD, such as progressive loss of striatal dopamine, alpha-synuclein pathology, deficits in motor and non-motor functions, and elevation of inflammatory markers. Extensive work with this model by multiple laboratories over the past decade further increased confidence in its robustness and validity, especially for analyzing pathomechanisms of alpha-synuclein pathology and down-stream pathways, and for pre-clinical drug testing. Interestingly, while postnatal transgene expression is widespread in central and peripheral neurons, the extent and progression of down-stream pathology differs between brain regions, thereby replicating the characteristic selective vulnerability of neurodegenerative diseases. In-depth characterization of these readouts in conjunction with behavioral deficits has led to more informative endpoints for pre-clinical trials. Each drug tested in Thy1-aSyn line 61 enhances knowledge on how molecular targets, pathology, and functional behavioral readouts are interconnected, thereby further optimizing the platform towards predictive validity for clinical trials. Here, we present the current state of the art using Thy1-aSyn line 61 for drug target discovery, validation, and pre-clinical testing.
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