To determine a potential mechanism for the observed increases in 25-OHC in ALS, we examined the mRNA expression of CH25H, CYP3A4, and CYP7B1 in the brain and spinal cord of transgenic mice with the human mutant SOD1 gene containing a glycine 93 (Gly93) to alanine (Ala) substation (mSOD1-G93A mice) at different time points (postnatal day of 60, 90, and 120) (Figure 9). This evidence concerns the gene SOD1 and amyotrophic lateral sclerosis.