TARDBP and amyotrophic lateral sclerosis: Studies in ALS, SBMA, MSP, and HSP (SPG11, SPG7) reveal constitutive activation or mislocalization of kinases such as p38 MAPK, JNK, and GSK3β, which results in pathological phosphorylation of tau, TDP-43, and neurofilaments, impairing intracellular trafficking and stimulating neurotoxicity [90].