Construction method and application of ALS mouse model with mitochondrial function damage
By selectively knocking out the Romo1 gene in mouse models, an ALS mouse model with mitochondrial function impairment was established, which solved the shortcomings of the existing models in pathological reproducibility and specific simulation, and achieved simulation of multidimensional phenotypes such as motor dysfunction and cognitive decline, which promoted the research on mechanisms of ALS and drug development.
Patent Information
- Application Number
- CN202510613019.1
- Authority / Receiving Office
- CN · China
- Patent Type
- Applications(China)
- Current Assignee / Owner
- Filing Date
- 2025-05-13
- Publication Date
- 2025-07-22
- Estimated Expiration
- Not applicable · inactive patent
AI Technical Summary
The existing ALS mouse models have insufficient pathological reproducibility in mitochondrial dysfunction, and are unable to effectively reproduce key clinical features such as cognitive decline, and lack models that specifically simulate mitochondrial damage to motor neurons, which affects disease mechanism research and drug development.
A mouse model with genotype Romo1flox/floxChatCre+ was constructed through the Cre/loxP system. The Romo1 gene was selectively knocked out in cholinergic neurons, spontaneously inducing amyotrophic lateral sclerosis, and an ALS mouse model with mitochondrial impairment was established.
This model not only reproduces movement disorders and progressive paralysis, but also simulates clinical multidimensional phenotypes such as cognitive decline, providing a pure research platform for mitochondria-specific mechanisms to help ALS pathogenesis and drug screening.