alpha-synuclein A53T Tg
This article summarizes the main uses, research targets, and related products of "alpha-synuclein A53T Tg," which is used in research on Parkinson's disease and Lewy body dementia.
Alpha-synuclein A53T Tg
Alpha-synuclein A53T Tg is a model overexpressing mutant alpha-synuclein (A53T), a gene responsible for familial Parkinson's disease in humans, under the control of a ubiquitous or neuron-specific promoter (such as Prp).
Overexpression of α-synuclein in the central nervous system reproduces Lewy body-like inclusions, motor deficits, and neurodegeneration. This model is widely used for research on Parkinson's disease and synucleinopathies, and is considered an important model for elucidating pathogenesis and evaluating therapeutic drugs.
The main subjects of research utilization
| Diseases for research |
How to use a disease model |
| Parkinson's disease (PD) |
Pathogenesis of familial Parkinson's disease (PARK1/PARK4) |
| Dementia with Lewy Bodies (DLB) |
Research on the formation of Lewy body-like aggregates in the brain and cognitive decline |
| Multiple System Atrophy (MSA) |
Research into synucleinopathies in general, characterized by the accumulation of alpha-synuclein in glial cells and neurons |
This model is frequently used for evaluations focusing on the "aggregation" and "neurotoxicity" of alpha-synuclein, rather than the degeneration of the dopaminergic system.
| How to use |
Details |
| Alpha-synuclein aggregation and accumulation analysis |
Quantification of insoluble α-synuclein (Western Blotting method)
Immunohistochemical observation of Lewy body-like structures by phosphorylated alpha-synuclein (Ser129) |
| Motor function assessment (motor function analysis) |
Rotarod Test: Measures Decreased Coordination Ability
Pole test: Assessment of bradykinesia
Grip Strength: Monitoring muscle strength and overall physical condition |
| Evaluation of neuroinflammation and synaptic toxicity |
Microglia and astrocyte activation (Iba1, GFAP staining)
Confirmation of reduced synaptic proteins (e.g., synaptophysin) in the striatum and cortex |
| Drug efficacy evaluation (drug discovery) |
Aggregation inhibitors: Screening of compounds that prevent the self-aggregation of α-synuclein
Antibody Drugs (Immunotherapy): Verification of the effect of anti-alpha-synuclein antibodies in removing aggregates and inhibiting intercellular transmission
Autophagy Activating Drugs: Confirmation of Neuroprotective Effects by Promoting the Degradation of Abnormal Proteins |
Review of alpha-synuclein A53T Tg
Proof of the causal relationship between A53T mutation and direct induction of toxic fibril formation and neurodegeneration
The paper "Neuronal alpha-synucleinopathy with severe movement disorder in mice expressing A53T human alpha-synuclein," published in 2002, describes the creation of transgenic mice that express A53T mutant human alpha-synuclein in neurons and the subsequent analysis of their pathology. This model develops severe movement disorders and paralysis with aging, leading to death. Furthermore, since a similar pathology did not occur in mice expressing wild-type human alpha-synuclein, this is considered an extremely important report that demonstrated in vivo the causative relationship by which the A53T mutation directly induces the formation of toxic fibrils and neuronal degeneration.
Key products of alpha-synuclein A53T Tg
Here, we introduce two products from the top 10 sites that appeared when searching for "alpha-synuclein A53T Tg products" on Google and where product pages could be confirmed (surveyed on May 14, 2026).
hA53Ttg Transgenic Mouse Model
Alpha-synuclein transgenic mice driven by the mouse Thy-1 promoter are an early-onset model. Since motor dysfunction is observed from 2 months of age, a significant reduction in the testing period is a major characteristic.
| Manufacturer/Distributor |
Analysis items |
Primary Endpoint |
| Scantox |
Motor function, cognitive function assessment, pSer129 α-synuclein quantification, NfL (neurofilament light chain), neuroinflammation |
Muscle weakness, motor impairment, and expression levels of alpha-synuclein and pSer129 alpha-synuclein |
RBRC02829
Transgenic mice expressing human alpha-synuclein under the control of the Th promoter. RBRC02829 express human alpha-synuclein with an Ala53Thr mutation and a deletion of the C-terminal 10 residues.
| Manufacturer/Distributor |
Analysis items |
Primary Endpoint |
| RIKEN Center for BioResource Research |
There was no information. |
There was no information. |
Summary
This article has introduced information regarding alpha-synuclein A53T Tg. In conducting non-clinical studies, selecting a reliable model is important. This site summarizes pathological models used in non-clinical studies, so please refer to the following articles as well.
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