This effect on neurons is evidenced by decreased axon degeneration and preserved neuromuscular junction (NMJ) in the ALS model [62] and, in the rat model of muscle overuse, by amelioration of mononeuropathy, decreased neural fibrosis and less sensory decline [104], opening the possibility of using CCN2/CTGF as a target for neurodegenerative diseases [21,103]. Here, CCN2 is linked to mononeuropathy.