4.3 Article

Amyotrophic Lateral Sclerosis and Oxidative Stress: A Double-blind Therapeutic Trial after Curcumin Supplementation

期刊

CNS & NEUROLOGICAL DISORDERS-DRUG TARGETS
卷 17, 期 10, 页码 767-779

出版社

BENTHAM SCIENCE PUBL
DOI: 10.2174/1871527317666180720162029

关键词

Amyotrophic Lateral Sclerosis (ALS); curcumin; oxidative stress; antioxidants; incremental exercise test; lactate

资金

  1. ALIVEDA Laboratory s.r.l.

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Objective: To investigate the efficacy of curcumin oral supplementation (600 mg/day, Bra noil), a natural antioxidant compound, in Amyotrophic Lateral Sclerosis (ALS). Methods: Patients were randomized into two groups: Group A received placebo for 3 months, then Brainoil for the following 3 months, Group B took Brainoil for 6 months. The evaluations were conducted at basal (TO), after 3 months of double blinded Brainoil or placebo treatment (T1), and after the 3 month open-label phase (T2). Clinical evaluations and oxidative stress biomarkers, including oxidative protein products (AOPPs), ferric reducing ability (FRAP), total thiols (T-SH) and lactate, were evaluated, compared to a control group, during an incremental forearm exercise test. Results: Over the entire study Group B showed a stable score of the ALS-FRS-r which decreased in Group A (p<0.01), in parallel with a reduction of AOPPs (p<0.01) which was not detected into Group A. Also FRAP exercise values remained stable in Group B, while in Group A they were reduced without treatment at T1>T0 exercise lactate was lower compared to Group A (p<0.01). Compared to controls, the whole ALS population showed a greater oxidative stress (p<0.001), those treated with curcumin (Group B) exhibiting decreased exercise AOPPs at T2 with values approaching those of controls. Conclusion: Although further studies are needed to confirm these data, treatment with curcumin shows encouraging results indicating a slight slowdown in disease progression, improving aerobic metabolism and oxidative damage, this also contributing to deepen knowledge into the pathogenic mechanisms of ALS.

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