Simvastatin accelerated motoneurons death in SOD1^G93A mice through inhibiting Rab7-mediated maturation of late autophagic vacuoles.

ABSTRACT: Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease caused by motoneuron loss, for which there is currently no effective treatment. Statins, as inhibitors of 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) reductase, are used as drugs for treatment for a variety of disease such as ischemic diseases, neurodegenerative diseases, cancer, and inflammation. However, our previous evidence has demonstrated that simvastatin leads to cytotoxicity in NSC34-hSOD1^G93A cells by aggravating the impairment of autophagic flux, but the role of simvastatin in ALS model remains elusive. In present study, we reported that after simvastatin treatment, SOD1^G93A mice showed early onset of the disease phenotype and shortened life span, with aggravated autophagic flux impa

SUBMITTER: Bai L 

PROVIDER: S-EPMC8041862 | biostudies-literature | 2021 Apr

REPOSITORIES: biostudies-literature