Alzheimer's Disease and Vitamin A low level

Alzheimer's disease (AD) is characterized by the presence of senile plaques composed of amyloid deposits consisting of aggregates of Aβ peptides and degeneration neurofibrillary cells caused by an accumulation and a hyperphosphorylation of protein tau.

Post-mortem results on patients’ brains with AD tend to confirm that the transport and route of the retinoids action is particularly altered in these subjects and suggest that decreased acid availability retinoic acid (AR, active metabolite of vitamin A) would promote the formation of amyloid (Goodman 2006, Maden 2007).

Among the essential nutrients brought by our food, vitamin A plays an important part. Indeed, it is involved in many fundamental processes such as embryonic development, vision, cell differentiation, immunity.

Recent scientist research has shown that reduced bioavailability of retinoic acid would, through a modification of the expression of genes coding for proteins involved in synaptic plasticity, contributes to the appearance of memory disorders associated with aging (Etchamendy et al. 2001).

Moreover, consistent data from the literature show that vitamin A deficiency in rodents leads in animals to impaired synaptic plasticity, neurogenesis, and memory deficits (Etchamendy et al., 2001; Etchamendy et al., 2003). (Bonnet et al., 2008) and the appearance of amyloid deposits (Corcoran et al., 2004) in cerebral vessels; these changes are considered markers of AD.

Vitamin A is a micronutrient that cannot be synthesized de novo by species of animal origin. This is why it must be brought by the diet. Vitamin A is found exclusively in animal products and is supplied as retinyl esters and to a lesser extent as retinol. The most important food sources are the livers, especially those of fish and marine mammals (cod, tuna, halibut ...), as well as the family's dairy products-eggs (butter, milk, cheese and eggs).

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