Efeitos bioquímicos da cafeína e a importância do receptor A3 para sua sinalização.

Abstract

Caffeine is part of a group of xanthines, called methylxanthines, is chemically known as 1,3,7-trimethylxanthine, and is the active ingredient in coffee. The vast majority of Brazilian adults consume daily doses of caffeine greater than 300 mg, and many can be considered drug-dependent individuals. It is mainly used because it causes an increase in alertness, the adenosinergic system seems to be more sensitive to the actions of caffeine, where it acts as a non-selective competitive antagonist of adenosine receptors (A1, A2A, A2B and A3), which belong to the family of G-protein-coupled proteins. Caffeine binds with greater affinity to adenosinergic receptors type A1 (inhibitory G protein-coupled) and A2A (stimulatory G protein-coupled). For some time it was believed that the A3 receptor was not very relevant to the effects of caffeine due to its high dissociation constant value. Activation of A3 receptors inhibits cAMP production through the action of an inhibitory G protein. In addition, phospholipase C activation is also described in rat brain after activation of this receptor. From a review of laboratory research and clinical research articles, it can be noted the importance of caffeine and the influence of the A3 receptor in some diseases that cause cognitive impairment, such as Alzheimer's disease. Alzheimer's disease is the neurodegenerative pathology most frequently associated with age, whose cognitive and neuropsychiatric manifestations result in progressive disability and disability. The disease affects approximately 10% of individuals over 65 years of age and 40% over 80 years of age. The biological effects of activation of A3 receptors by adenosine are still under investigation, but there is evidence that these receptors are the mediators of several of the effects associated with caffeine. In vitro studies with neurons indicate that caffeine, by antagonizing A3 receptors, prevents the internalization of the amyloid beta protein precursor. Apparently, by inhibiting this internalization, the generation of mature beta amyloid protein, which is the protein responsible for degeneration in Alzheimer's disease (AD), is reduced.