TGF-β has been characterized as an injury-responsive factor and subsequently as a disease modulator in the central nervous system (CNS) based on the observation that among three TGF-β ligands, TGF-β1 increases acutely after brain injury, including trauma, ischemia, and encephalitis, and chronically in many neurodegenerative diseases, including AD, Parkinson’s disease, and amyotrophic lateral sclerosis (ALS) [88,89,90]. This evidence concerns the gene TGFB1 and amyotrophic lateral sclerosis.