We observed increased SIRT1 levels in symptomatic ALS SOD1G93A transgenic mice and found that SIRT1 not only is a crucial molecule for orexin synthesis but also directly interacts with increased levels of prepro-orexin in the hypothalamus in both presymptomatic and symptomatic SOD1G93A transgenic mice. The gene discussed is HCRT; the disease is amyotrophic lateral sclerosis.