Amyotrophic Lateral Sclerosis (ALS) Model 

Transgenic SOD1 (superoxide dismutase 1) mice express a G93A mutant form of human SOD1. SOD1 mice (TgN-SOD1-G93A-1Gur) exhibit a phenotype similar to amyotrophic lateral sclerosis (ALS) in humans, an age-related rapidly progressive decline of motor functions accompanied by degenerative changes of motoneurons within the spinal cord, brain stem and neocortex. Charles River Discovery Research Services has negotiated the license to employ the transgenic material from Northwestern University/Harvard/MIT for third parties. All characterization and analytical methods used with the model are performed in our proprietary labs by our own staff of scientists and technicians.

Example Study Paradigm of ALS Mouse Model

Click here to view an example study paradigm of our transgenic SOD1 (superoxide dismutase 1) mouse model of ALS.

Study Components with SOD1 Mice

• Body weight
• Kaplan-Meyer survival plot
• Motor deficits
• Open field test
• Distance traveled
• Rearing frequency
• Rotarod
• Grip strength
• Clinical scoring for disease state

Optional Study Components with SOD1 Mice 

• MRI for neurodegeneration in the brain stem
• MRS for metabolic changes in the brain stem
• Motor neuron counts

For more information about our transgenic SOD1 mouse model for ALS research, please contact us at 1.877.CRIVER.1 or askcharlesriver@crl.com.

Charles River also offers an in vitro ALS model that is created by exposing a spinal cord cell culture to Kainic acid. For more information, click here.