Related Experiment Video
Updated: Apr 26, 2026
Assessment of Sensorimotor Function in Mouse Models of Parkinson's Disease
Published on: June 17, 2013
Tetranectin knockout mice develop features of Parkinson disease
Er-song Wang1, Xiao-ping Zhang, Hui-bin Yao
1Department of Neurosurgery, Jinshan Hospital, Fudan University, Shanghai, China.
Background/Aims:
Aggregation of insoluble α-synuclein to form Lewy bodies (LBs) may contribute to the selective loss of midbrain dopaminergic neurons in Parkinson disease (PD). Lack of robust animal models has impeded elucidation of the molecular mechanisms of LB formation and other critical aspects of PD pathogenesis.
Methods:
We established a mouse model with targeted deletion of the plasminogen-binding protein tetranectin (TN) gene (TN(-/-)) and measured the behavioral and histopathological features of PD.
Results:
Aged (15-to 20-month-old) TN(-/-) mice displayed motor deficits resembling PD symptoms, including limb rigidity and both slower ambulation (bradykinesia) and reduced rearing activity in the open field. In addition, these mice exhibited more numerous α-synuclein-positive LB-like inclusions within the substantia nigra pars compacta (SNc) and reduced numbers of SNc dopaminergic neurons than age-matched wild type (WT) mice. These pathological changes were also accompanied by loss of dopamine terminals in the dorsal striatum.
Conclusion:
The TN(-/-) mouse exhibits several key features of PD and so may be a valuable model for studying LB formation and testing candidate neuroprotective therapies for PD and other synucleinopathies.
Insights
Mice lacking tetranectin (TN) developed Parkinson disease (PD) symptoms, including motor deficits and Lewy body-like inclusions. This new TN(-/-) mouse model aids Parkinson disease research.
Area of Science:
- Neuroscience
- Genetics
- Pathology
Background:
- Alpha-synuclein aggregation into Lewy bodies (LBs) is implicated in Parkinson disease (PD) pathogenesis.
- Loss of midbrain dopaminergic neurons is a hallmark of PD.
- A lack of suitable animal models hinders the study of LB formation and PD.
Purpose of the Study:
- To establish and characterize a novel mouse model for Parkinson disease.
- To investigate the role of tetranectin (TN) in PD pathogenesis.
- To evaluate the utility of the TN(-/-) mouse model for studying LB formation and neuroprotection.
Main Methods:
- Generation of a tetranectin (TN) gene knockout mouse model (TN(-/-)).
- Assessment of behavioral and histopathological features relevant to PD.
- Analysis of motor deficits, LB-like inclusions, dopaminergic neuron counts, and dopamine terminal loss.
Main Results:
- Aged TN(-/-) mice exhibited motor impairments, including rigidity and bradykinesia.
- TN(-/-) mice showed increased α-synuclein-positive LB-like inclusions in the substantia nigra pars compacta (SNc).
- Reduced SNc dopaminergic neurons and dorsal striatum dopamine terminals were observed in TN(-/-) mice compared to wild type.
Conclusions:
- The TN(-/-) mouse model recapitulates key pathological and clinical features of Parkinson disease.
- This model provides a valuable tool for investigating LB formation mechanisms.
- The TN(-/-) mouse is suitable for testing potential neuroprotective therapies for PD and other synucleinopathies.
Related Concept Videos
01:24Parkinson Disease ll: Pathophysiology
01:16In-vitro Mutagenesis
01:24Parkinson's Disease: Treatment
Parkinson's Disease is primarily a result of the loss of dopaminergic neurons in the substantia nigra pars compacta. The cornerstone of...