Delayed Symptom Onset and Prolonged Survival Time in ALS Model Mice through the Inhibition of GSK-3 Activity

Abstract

The primary pathogenic mechanism of amyotrophic lateral sclerosis (ALS) remains largely unclear. We recently reported that motoneuron cell death mediated by G93A or A4V mutant SOD1, causing familial ALS, was related with decrease of survival signals, such as phosphatidylinositol-3-kinase (PI3-K) and Akt, and increase of death signals, such as GSK-3. This study was undertaken to evaluate the effect of GSK-3 activity on morphological change of spinal cord, symptom onset, and survival time in ALS model mice.