Neuronutrition and Alzheimer's disease

Abstract

Alzheimer's disease (AD) is a complex neurological disorder resulting from both genetic and environmental factors with the latter being particularly important for the sporadic form of the disease. As such, diets rich in saturated fatty acids and alcohol, and deficient in antioxidants and vitamins appear to promote the onset of the disease, while diets rich in unsaturated fatty acids, vitamins, antioxidants, and wine likely suppress its onset. In addition, evidence suggests that diets rich in polyphenols and some spices suppress the onset of AD by scavenging free radicals and preventing oxidative damage. Metal ions are known to catalyze the production of free radicals and induce mental retardation or dementia, and several studies have also identified metals such as Pb, Fe, Al, Cu, and Zn in AD pathogenesis. While specific metal chelators have been tested for therapy, they have not been very successful, probably due to their late administration, i.e., after brain damage has been triggered. Since several dietary polyphenols are known to chelate metals, their routine use may also be protective against the onset of AD. In this review, we summarize beneficial dietary techniques in the fight against AD.

Figure 1

The role of homocysteine in AD: Vitamin B6 acts as a cofactor in the maintenance of homeostasis between homocysteine and cysteine. Any imbalance in the vitamin B6 levels alters the balance between homocysteine to cysteine. The higher homocysteine levels may cause insufficient DNA repair leading to accumulation of DNA strand breaks. This may lead to neuronal cell dysfunction.

Figure 2

EGCG's mode of action: Environmental factors such as metals cause oxidative stress, leading to protein, lipid, and DNA damage. EGCG is known to chelate transition metals like Fe and Cu, there by prevents oxidative stress. EGCG also acts as an anti-inflammatory molecule and increases the activity of SOD and Catalase. EGCG induces the PI3K/Akt-signaling pathway, and this pathway has a pivotal role in neuronal cell survival.

Figure 3

The role of resveratrol in modulating neurodegeneration: Resveratrol favors phosphorylation in PKC. This activates the non-amyloidogenic pathway of AβPP cleavage, and this leads to reduction in Aβ formation. sAβPPα, which is a product of AβPP cleavage, gets translocated to the nucleus and modulate the genes. Resveratrol also nonspecifically stimulates proteosomes, which helps in clearing Aβ. All these events favor neuronal cell survival.

Figure 4

The diverse effects of curcumin in combating neurodegeneration: Curcumin has multiple biological effects. It chelates transition metals (Fe and Cu) and acts as an antioxidant and anti-inflammatory molecule. Curcumin may protect the cells from oxidative stress.