Table 1.
Summary of nutritional supplements and principal effects in different study models of Alzheimer’s disease.
| Treatment | Model of Study | Time | Effects/Outcome | Refs. |
|---|---|---|---|---|
| Vitamin E | Rat | 4 months | -Upregulation of genes involved in resistance to oxidative stress counteraction of the effects of fluid percussion injury | [23] |
| Vitamin E | AD mouse model | 1 month | -Decreased brain lipid peroxidation levels-Attenuated learning deficits | [24] |
| Vitamin E + Vitamin C | Human, elderly population | 5 years follow-up | -Reduced prevalence and incidence of AD | [26] |
| Vitamin E + Vitamin C + β-carotene | Human, meta-analysis | -Lower risk of AD-Vitamin E plays the pivotal role | [28] | |
| Vitamin E ± Vitamin C | Dementia-free community | 13 years follow-up | -No delay in dementia or AD incidence | [33] |
| Vitamin E | Dementia-free community | 5.5 years follow-up | -No protective role against dementia | [34] |
| Vitamin E | Human, MCI patients | 3 years | -No affection of disease progression | [35] |
| Vitamin E | Human, AD patients | 6 months | -Cognitive status maintenance, in patients where Vit E lowered oxidative stress status-Detrimental cognitive effects, in patients where Vit E did not affect oxidative stress status | [36] |
| Fig | AD mouse model | 15 months | -Reduction of plasma Aβ(1-40) and Aβ(1-42)-Enhanced activity of antioxidant enzymes in cortex and hippocampus | [40] |
| Fig | AD mouse model | 15 months | -Improvement of cognitive and behavioral deficits | [41] |
| Resveratrol | Age-related AD mouse model | 2 months | -Increased mean life expectancy and life span-Decreased amyloid burden and reduced tau hyper phosphorylation | [45] |
| Alcohol-free wine | Human, young volunteers | 1 week | - the activity of the antioxidant enzymes is not dueto the alcohol content in wine but to the polyphenolic composition | [46] |
| Ginkbo Biloba extract (EGb 761) | Rat | 2 weeks | -Cardio protective effect-Inhibition of free radical formation | [47] |
| Ginkbo Biloba extract (EGb 761) | N2a cell line stably expressing Swedish mutant APP695 and the exon-9 deletion mutant PS1 | -Neuroprotective effects (e.g. attenuation of apoptosis and direct inhibition of Aβaggregation) | [48] | |
| Ginkbo Biloba extract (EGb 761) | Human | 6.1 years follow-up | -Not effective in reducing either the overall incidence rate of dementia or AD incidence | [49] |
| ω3 fatty acids | Mild to moderate AD patients | 6 months | -No effects in the rate of cognitive decline | [125] |
| ω3 fatty acids | Mild to moderate AD patients | 6 months | -Positive effect on weight and appetite | [68] |
| ω3 fatty acids | Mild to moderate AD patients | 6 months | -Blood mononuclear monocytes up-regulation of genes involved in inflammation and neurodegeneration | [128] |
| ω3 fatty acids | Mild to moderate AD patients | 6 months | -No clear effect on free radical-mediated formation of F2-isoprostane or cyclooxygenase-mediated formation of prostaglandin F2α | [63] |
| ω3 fatty acids | AD mouse model | 7 months | -No protection against AD development in high-risk individuals | [129] |
| ω3 fatty acids | MCI and mild to moderate AD patients | 24 weeks | -Improvement in ADAS-cog in MCI patients but not in AD patients | [65] |
| Souvenaid | Mild AD patients | 12 weeks | -Memory improvement (delayed verbal recall) | [120] |
| Souvenaid | Mild AD patients | 24 weeks | -Good tolerance-Improvement of memory performance | [118] |
| Souvenaid | Mild to moderate AD patients | 24 weeks | -No slowing down of cognitive decline-Well tolerated in combination with standard AD medication | [121] |
| Souvenaid | Mild AD patients | 24 weeks | -Preservation of the organization of brain networks | [117] |