CTRL and amyotrophic lateral sclerosis: Neuroprotective in primary motor neurons by inhibition of the secretion of Substance P and IL-1β and mitochondrial dysfunction by inhibiting the release of cytochrome c/Smac/AIF and activation of apoptotic pathways (caspase-1, -9, and -3), as well as proteasomal dysfunction through restoring chymotrypsin-like, trypsin-like, and caspase-like proteasome activity in ALS.