ALS Mouse Model Crossing Study
Objective: To evaluate the protective effects of Nrf2 activation in astrocytes on disease onset and survival in ALS mouse models by crossing GFAP-Nrf2 transgenic mice with two ALS-mouse models
This is a ALS Mouse Model Crossing Study protocol using mouse as the model organism. The procedure involves 4 procedural steps, 1 materials. Extracted from a 2008 paper published in Journal of Neuroscience.
Model and subjects
mouse • GFAP-Nrf2 transgenic mice crossed with ALS-mouse models • unknown • Not specified • Not specified
Study window
Estimated timing pending
Core workflow
Generate transgenic mice • Cross GFAP-Nrf2 mice with ALS-mouse models • Monitor disease onset
Primary readouts
- Disease onset timing
- Survival duration
- Motor neuron protection
- Glutathione secretion from astrocytes
Key equipment and reagents
Verified items
0
Direct vendor links
0
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Protocol Steps
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Generate transgenic mice
Generated transgenic mice over-expressing Nrf2 selectively in astrocytes using the glial fibrillary acidic protein (GFAP) promoter
Note: GFAP promoter used for astrocyte-specific expression
View evidence from paper
“We generated transgenic mice over-expressing Nrf2 selectively in astrocytes using the glial fibrillary acidic protein (GFAP) promoter”
Cross GFAP-Nrf2 mice with ALS-mouse models
Crossed the GFAP-Nrf2 mice with two different ALS-mouse models to evaluate protective effects
Note: Two separate ALS-mouse models were used
View evidence from paper
“This protective effect was also observed by crossing the GFAP-Nrf2 mice with two ALS-mouse models”
Monitor disease onset
Monitored and recorded the onset of disease symptoms in crossed mice
Note: Nrf2 over-expression in astrocytes significantly delayed onset
View evidence from paper
“Over-expression of Nrf2 in astrocytes significantly delayed onset and extended survival”
Monitor survival
Tracked and recorded survival duration in crossed mice
Note: Nrf2 over-expression extended survival in ALS models
View evidence from paper
“Over-expression of Nrf2 in astrocytes significantly delayed onset and extended survival”