No benefit of dietary restriction on disease onset or progression in amyotrophic lateral sclerosis Cu/Zn-superoxide dismutase mutant mice

Ward A. Pedersen, Mark P. Mattson

Research output: Contribution to journalArticle

Abstract

Amyotrophic lateral sclerosis (ALS) is a fatal disease in which spinal cord motor neurons degenerate resulting in progressive paralysis. Some cases of ALS are caused by mutations in the antioxidant enzyme Cu/Zn-superoxide dismutase (SOD). Transgenic mice expressing ALS-linked Cu/Zn-SOD mutations (SODMutM) exhibit a phenotype analogous to that of human ALS patients. Dietary restriction (DR) is a well-established means of extending lifespan in rodents. It may act by reducing levels of cellular oxidative stress. We therefore tested the hypothesis that DR will retard the development of the clinical phenotype and extend the lifespan of SODMutM. There was no significant difference in age of disease onset in mice placed on a DR regimen beginning at 6 weeks of age compared to mice fed ad libitum, and disease duration was shortened indicating that DR accelerates the clinical course. Histological analyses indicated a similar extent of lower motor neuron degeneration in SODMutM maintained on DR or ad libitum diets. We conclude that a dietary manipulation known to extend lifespan has no beneficial effect in an animal model of familial ALS.

Original languageEnglish (US)
Pages (from-to)117-120
Number of pages4
JournalBrain Research
Volume833
Issue number1
DOIs
StatePublished - Jun 26 1999
Externally publishedYes

Keywords

  • Amyotrophic lateral sclerosis
  • Antioxidant enzyme
  • Caloric restriction
  • Motor neuron
  • Oxidative stress

ASJC Scopus subject areas

  • Neuroscience(all)

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