Oxidative stress and mitochondrial damage in the pathogenesis of ALS: New perspectives

F. Bozzo, A. Mirra, M. T. Carrì

Research output: Contribution to journalArticlepeer-review

Abstract

This review attempts to reconcile the present dual view of the mechanisms operating in Amyotrophic Lateral Sclerosis (ALS). On one side, oxidative stress, mitochondrial damage and protein aggregation are considered as causative of the disease, as strongly supported by evidence obtained in models based on the expression of ALS-typical mutant SOD1. On the other hand, evidence from models expressing ALS-typical mutations in RNA-binding proteins such as FUS and TDP43 indicate that mRNA (dys)metabolism is a major pathway in this disease. A critical analysis of existing literature suggests that there may be more than one point of intersection.

Original languageEnglish
JournalNeuroscience Letters
DOIs
Publication statusAccepted/In press - Jan 26 2016

Keywords

  • ALS
  • FUS/TLS
  • Iron
  • Mitochondria
  • Oxidative stress
  • RNA metabolism
  • SOD1
  • TDP43

ASJC Scopus subject areas

  • Neuroscience(all)

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