Nevertheless, the lack of an immune activation response supporting leukocyte trafficking in the CP of the SOD1G93A ALS mouse model [43] is consistent with our human ALS-CP data where we observed significant downregulation of the M-CSF cytokine and the VCAM-1 leukocyte transendothelial migration marker. This evidence concerns the gene CSF1 and amyotrophic lateral sclerosis.