The brain specific isoform (JNK3) of c-Jun NH2-terminal kinase (JNK) has been found to mediate the degeneration of spinal motor neurons caused by SMN deficiency in spinal muscular atrophy (SMA). Moreover, the ability of JNK inhibitors to reduce degeneration of neurons lacking SMN is also disclosed. The JNK signaling pathway can therefore mediate neurode-generation in SMA and represents a therapeutic target for treatment of SMA.
