Abstract

 

Epidemiological and experimental studies support the beneficial effect of habitual caffeine consumption in Alzheimer's Disease (AD). The underlying mechanisms remain however ill-defined but are thought to depend on its ability to block adenosine A2A receptors, found upregulated in hippocampal neurons and astrocytes of AD patients. I will highlight recent data from our group that demonstrate the ability of caffeine to promote molecular mechanisms associated with efficient hippocampal-dependent memory. In addition, I will share findings which support that the dysregulation of the caffeine receptors in the brain of AD patients is instrumental to neuroglial impairments leading to synaptic and memory deficits. Based on these experimental data, current and expected translational development will be discussed.

 

Dr David Blum
Lille University