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.