The accumulation of SOD1G93A in the spinal cord and neurons serves as a molecular marker of the progression of ALS in SOD1G93A mice, beginning at 2 months of age; the aggregation of human SOD1G93A protein is observed in the white and gray matter of the lumbar spine, accompanied by increased levels of glial fibrillary acidic protein (GFAP) and neuromuscular symptoms such as decreased muscle strength, which are indicative of neuromuscular degeneration. This evidence concerns the gene GFAP and amyotrophic lateral sclerosis.