Given the observed increase in PGC-1α expression following BMD-001S treatment, these findings suggest that BMD-001S may exert anti-inflammatory and neuroprotective mechanisms by enhancing PGC-1α activity [25], thereby facilitating clearance of toxic SOD1 aggregates and reducing neurodegeneration in the spinal cord of SOD1G93A-induced ALS. This evidence concerns the gene SOD1 and amyotrophic lateral sclerosis.