| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 1906517 | Experimental Gerontology | 2012 | 5 Pages |
A randomized, double-blind placebo-controlled clinical trial was carried out to assess the efficacy of a docosahexenoic acid (DHA)-phospholipids, melatonin and tryptophan supplemented diet in improving the erythrocyte oxidative stress, membrane fluidity and membrane-bound enzyme activities of elderly subjects suffering from mild cognitive impairment (MCI). These subjects were randomly assigned to the supplement group (11 subjects, 9F and 2M; age 85.3 ± 5.3 y) or placebo group (14-matched subjects, 11F and 3M; 86.1 ± 6.5). The duration of the treatment was 12 weeks. The placebo group showed no significant changes in erythrocyte membrane composition and function. The erythrocyte membranes of the supplement group showed a significant increase in eicosapentenoic acid, docosapentenoic acid and DHA concentrations and a significant decrease in arachidonic acid, malondialdehyde and lipofuscin levels. These changes in membrane composition resulted in an increase in the unsaturation index, membrane fluidity and acetylcholine esterase activity. Moreover, a significant increase in the ratio between reduced and oxidized glutathione was observed in the erythrocyte of the supplement group.Although this study is a preliminary investigation, we believe these findings to be of great speculative and interpretative interest to better understand the complex and multi-factorial mechanisms behind the possible links between diets, their functional components and possible molecular processes that contribute to increasing the risk of developing MCI and Alzheimer's.
► 25 MCI patients were randomized to diet integration or placebo for 12 weeks. ► Diet was supplemented with DHA-phospholipids, melatonin and tryptophan. ► Changes in erythrocyte membrane composition, fluidity and redox state were evaluated. ► Supplementation improves erythrocyte chemico-physical and functional properties. ► Links between MCI brain malfunction and diet-induced membrane changes are discussed.
