Histopathological analysis of the lumbar spinal cord (L4 and L5) revealed that the lack of Lpar2 did not have any effect on motoneuron survival in ALS mice (Figures 5A,B) despite electrophysiological tests revealing that the amplitude of the CMAPs was significantly increased in ALS mice deficient in Lpar2 at 16 weeks of age (Figures 5C–F). Here, LPAR2 is linked to amyotrophic lateral sclerosis.