| Autor: |
Boumil, Edward F., Vohnoutka, Rishel Brenna, Liu, Yuguan, Lee, Sangmook, Shea, Thomas B |
| Zdroj: |
The Open Neurology Journal; December 2017, Vol. 11 Issue: 1 p84-91, 8p |
| Abstrakt: |
Background:Amyotrophic lateral sclerosis (ALS) is a progressive disease of motor neurons that has no cure or effective treatment. Any approach that could sustain minor motor function during terminal stages would improve quality of life.Objective:We examined the impact of omega-3 (Ω-3) and Ω-6, on motor neuron function in mice expressing mutant human superoxide dismutase-1 (SOD-1), which dominantly confers familial ALS and induces a similar sequence of motor neuron decline and eventual death when expressed in mice.Method:Mice received standard diets supplemented with equivalent amounts of Ω-3 and Ω-6 or a 10x increase in Ω-6 with no change in Ω-3 commencing at 4 weeks of age. Motor function and biochemical/histological parameters were assayed by standard methodologies.Results:Supplementation with equivalent Ω-3 and Ω-6 hastened motor neuron pathology and death, while 10x Ω-6 with no change in Ω-3 significantly delayed motor neuron pathology, including preservation of minor motor neuron function during the terminal stage.Conclusion:In the absence of a cure or treatment, affected individuals may resort to popular nutritional supplements such as Ω-3 as a form of “self-medication”. However, our findings and those of other laboratories indicate that such an approach could be harmful. Our findings suggest that a critical balance of Ω-6 and Ω-3 may temporarily preserve motor neuron function during the terminal stages of ALS, which could provide a substantial improvement in quality of life for affected individuals and their caregivers. |
| Databáze: |
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