Vitamine A et vieillissement cérébral

Abstract

To date, convergent data on the role of retinoic acid in the mature brain have established that this molecule, which acts as a hormone, helps to preserve cerebral plasticity by controlling dendritic spine density as well as hippocampal neurogenesis. Deterioration in cerebral plasticity seems to be at the base of the cognitive decline disease. Furthermore, the transcription of several genes, known as muted, in Alzheimer’s patients and whose transcripts are involved in the formation of senile plaques, are controlled by retinoic acid. As seen in other nutrients, aging leads to a lower production of retinoic acid; a phenomenon probably accentuated by the fact that Western populations consume an insufficient amount of vitamin A (60% of the population has a consumption lower than the recommendations). These two phenomena (i.e. level of consumption, the lack of activation of vitamin A) accompanied by important individual differences, would help to explain why some patients have an almost normal aging process, whereas others gradually develop cognitive disorders and then, the disease. A better understanding of the role of a collapse of the retinoid status in the genesis of Alzheimer lesions could, beyond the definition of a preventive nutritional strategy, open therapeutic perspectives, through the use of molecules targeting the nuclear receptors.

Keywords

• aging
• brain
• memory
• Retinoic acid nuclear receptors (RAR, RXR)
• Alzheimer’s disease