One of the main features of Alzheimer's disease (AD) is a dysfunction in the metabolism of glucose in the brain. These alterations can be observed in very early stages of the disease, even decades before clinical symptoms. It has been postulated that these metabolic changes could be related to synaptic alterations and cognitive decline.

Moreover, several studies have shown that diet can modulate neuronal function, either negatively (on diets high in saturated fat and sugars) or positively (on diets rich in fruits and vegetables, polyunsaturated fatty acids and fibers). In our laboratory we have particular interest in elucidating the effect of different foods on the metabolic expenditure and neuronal function, both in models of obesity and Alzheimer's disease.

We have observed that various foods can prevent or delay the deterioration of memory, by increasing the metabolic rate of specific type of cells. This could help to develop therapeutic strategies to prevent the development of dementia and Alzheimer's disease.

We are also interested in developing drugs that modify the course of Alzheimer's disease.

On the other hand, we want to characterize non-transgenic models of AD, such as non-human primates (common marmoset). These models have the advantage of presenting a closer human genome sequence, as well as a more complex and developed brain compared to rodents.