No benefit of dietary restriction on disease onset or progression in amyotrophic lateral sclerosis Cu/Zn-superoxide dismutase mutant mice.
Level 5 - mechanism / opinion, no new human data
Animal research (SOD1 transgenic mouse model)
PubMed 10375685 · doi:10.1016/s0006-8993(99)01471-7
What was done
Transgenic mice expressing ALS-linked Cu/Zn-superoxide dismutase mutations (SODMutM) were placed on a dietary restriction regimen or an ad libitum diet starting at 6 weeks of age. Researchers evaluated the effects of dietary restriction on age of disease onset, clinical disease duration, and lower motor neuron degeneration assessed by histological analysis.
What was found
The abstract reports no exact numbers. There was no significant difference in age of disease onset between mice on dietary restriction and those fed ad libitum. Disease duration was shortened in the dietary restriction group, indicating that dietary restriction accelerates the clinical course. Histological analyses showed a similar extent of lower motor neuron degeneration in both groups.
Why it matters
This study shows that dietary restriction, an intervention known to extend lifespan in healthy rodents, provides no neuroprotection and may accelerate disease progression in a genetic model of familial ALS.
Limits
This is an animal model study in mutant mice and cannot be directly translated to human ALS. The abstract does not report the sample size, exact quantitative measurements for onset or survival, or the specific dietary restriction protocol.
Cited by
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