Food restriction-induced autophagy modulates degradation of mutant SOD1 in an amyotrophic lateral sclerosis mouse model

•LC3II and p62 increased in lumbar spinal cord of ALS mice.•Food restriction reduced p62 and mutant SOD1 at onset stage.•Activating autophagy at certain disease stage may be protective.

Autophagy dysregulation has been implicated in the pathogenesis of amyotrophic lateral sclerosis (ALS). The expression of LC3II and sequestosome 1 (P62) was progressively increased in the lumbar spinal cord of ALS mice. However, whether autophagy is activated or inhibited is still unclear. By treating mice with food restriction, a well-recognized way to induce autophagy, we found that 48 h of food restriction significantly reduced p62 and mutated SOD1 expressions at onset stage but not at pre-end stage in the spinal cord of SOD1-G93A mice. These data indicate that activating autophagy at a certain disease stage may have potential protective effects on ALS.