European Journal of Inflammation (Sep 2014)
Alzheimer's Disease: From Genes to Nutrition
Abstract
Alzheimer's disease (AD) is widely identified as the most common cause of sporadic dementia. Its aetiology is still debated, as despite several hypotheses, different factors seem to play a role in its establishment and development. Recent studies have proposed a possible preventing role of nutrition. The weight loss typical of earlier phase of disease and the finding of malnutrition as a common trait between patients leads to hypothesize that a supplementation of specific nutrients seems to be useful and effective in terms of improvement of cognitive functions. Malnourished patients show also altered parameters when investigating inflammation markers: for example, hyperhomocysteinemia is a typical finding in elderly affected by dementia, and it can be prevented and corrected by using a proper nutrients supplementation. Pro-inflammatory state can be reduced with supplementation of polyunsaturated fatty acids, vitamins of the group B and phosphatidylserine, that can act reducing IL-1β (pro-inflammatory cytokine) and improving IL-10 (anti-inflammatory cytokine) synthesis. While investigating the role of nutrition, it seems to be deeply linked with genetic; a genetic onset AD-related could be latent and can be influenced by nutritional attitude. AD can be considered a sort of latent clinical condition that would disclose or not, depending also on micro-environment and nutritional parameters. The genetic expression can be influenced by assumptions or not of specific nutrients, with the promotion of different pro- or anti-inflammatory settings. The specific role of each micronutrient (in particular vitamins) and trace elements still needs to be punctuated, as they are involved in a pool of different reactions. Also genes acts not independently but in an interconnected pattern, in which the role of a single gene needs to be cleared, depending on others. This complex system of predisposing conditions and a possible role of nutrition as modulator of the inflammatory state is the object of this review.