hA53T-α-syn induced Mouse Model Development Service
Parkinson's disease (PD) is a progressive neurodegenerative disorder characterized by the loss of dopaminergic neurons in the substantia nigra and the accumulation of aggregated α-synuclein protein. The hA53T mutation in the α-synuclein gene is associated with familial forms of PD, making it a relevant target for disease modeling. The hA53T-α-synuclein induced mouse model has been widely used to investigate the pathogenesis of PD and to evaluate potential therapeutic strategies. Research has shown that this model recapitulates key features of PD, including motor deficits, dopaminergic neurodegeneration, and α-synuclein pathology. Our hA53T-α-syn Induced Mouse Model helps you accelerate your research and obtain more translational results through the precise modeling of key pathological features of PD.
How Our hA53T-α-syn Induced Mouse Model Can Assist Your Project?
Creative Biolabs' hA53T-α-syn Induced Mouse Model provides researchers with a robust platform for investigating PD pathogenesis and evaluating potential therapeutic interventions. This model offers a range of deliverables and solutions, including:
- Accurate Disease Modeling: Clients can expect a model that recapitulates key pathological hallmarks of PD, including α-synuclein aggregation, dopaminergic neurodegeneration, and neuroinflammation.
- Efficacy Testing: The model enables the in vivo assessment of novel therapeutic compounds, allowing for the evaluation of their efficacy in modifying disease progression and alleviating symptoms.
- Target Validation: Researchers can utilize the model to validate potential drug targets and explore the underlying mechanisms of PD.
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Workflow
We employ a rigorous and well-defined workflow for generating and utilizing the hA53T-α-syn Induced Mouse Model:
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Required Starting Materials:
- Client provides the specific therapeutic compounds to be tested.
- Client specifies the desired study design, including dosing regimens, treatment duration, and endpoints.
- Client outlines any specific research questions or objectives.
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Final Deliverables:
- Detailed study report with comprehensive data analysis.
- Quantifiable data on behavioral changes, dopaminergic neuron loss, α-synuclein pathology, and neuroinflammation.
- Histological images and biomarker measurements.
- Estimated Timeframe: The typical timeframe for this service ranges from 8 to 16 weeks, depending on the specific study design, treatment duration, and complexity of the endpoints.
Why Choose Us?
CBL stands out as a premier provider of preclinical PD models due to our:
- Expertise: CBL has extensive experience in generating and characterizing the hA53T-α-synuclein induced mouse model. Our team of scientists possesses in-depth knowledge of PD pathogenesis and animal model development.
- Customization: We offer flexible study designs tailored to your specific research needs, ensuring that the model effectively addresses your research questions.
- Comprehensive Services: CBL provides a complete range of services, from model generation to data analysis and reporting, streamlining your research process.
- Quality and Reliability: We adhere to the highest scientific standards, ensuring the quality and reliability of our models and data. Published Data supports the validity and reliability of our models.
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hA53T-α-syn Induced Mouse Model
The hA53T-α-synuclein induced mouse model is a valuable tool for PD research, as demonstrated by its ability to replicate several key pathological features of the disease.
Fig.1 AAV1/2-A53T-aSyn SN injection leads to motor deficits and widespread aSyn expression and aggregation.1
Customer Reviews
"Using CBL's hA53T-α-synuclein model in our research has significantly improved the translatability of our preclinical findings to human PD." [10 Weeks], J***es
"CBL's hA53T-α-synuclein model allowed us to efficiently evaluate the efficacy of our therapeutic compound on key PD-related endpoints." [14 Weeks], S***h
"The level of detail and support provided by CBL throughout the study was exceptional. The data generated from the hA53T-α-synuclein model was of high quality and directly applicable to our research." [12 Weeks], M***n
What We Can Offer
We offer biology experts a comprehensive solution for their PD research needs. Our hA53T-α-synuclein Induced Mouse Model service includes:
- Precise generation of hA53T-α-synuclein induced mouse models, ensuring accurate recapitulation of key PD pathological features.
- Customizable study designs, including variations in AAV serotypes, injection sites, and expression levels, to meet specific research objectives.
- Comprehensive in vivo pharmacology services, including compound administration, behavioral testing, and efficacy assessments.
- Detailed histological and biochemical analyses, including immunohistochemistry, stereology, and biomarker quantification.
- Flexible options for tissue sampling, biofluid collection, and other ex vivo analyses.
- Expert consultation and support throughout the study, from initial design to final report.
- Stringent quality control measures to ensure data reproducibility and reliability.
- Ability to incorporate cutting-edge technologies, such as gene therapy, into study design.
- Assistance with data interpretation and preparation for publication or regulatory submission.
- Options for long-term studies, model maintenance, and breeding.
Related Services
CBL offers a range of complementary services that can support your PD research:
FAQs
Q How does the hA53T-α-synuclein model compare to other PD models?
Q What are the typical endpoints measured in studies using the hA53T-α-synuclein model?
Q What are the advantages of using CBL for my hA53T-α-synuclein model study?
Q Are there any special precautions when working with the hA53T-α-synuclein model?
Q Can CBL help with data analysis and interpretation?
Reference
- Ip, Chi Wang, et al. "AAV1/2-induced overexpression of A53T-α-synuclein in the substantia nigra results in degeneration of the nigrostriatal system with Lewy-like pathology and motor impairment: a new mouse model for Parkinson's disease." Acta neuropathologica communications 5 (2017): 1-12.. Distributed under Open Access license CC BY 4.0, without modification.

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