Epidemiologic studies suggest an inverse correlation between coffee consumption and the occurrence ofneurodegenerative diseases, but the role of caffeine and roasting degree are still matter of debate. The objective of this workwas to evaluate the eff...
Epidemiologic studies suggest an inverse correlation between coffee consumption and the occurrence ofneurodegenerative diseases, but the role of caffeine and roasting degree are still matter of debate. The objective of this workwas to evaluate the effects of caffeinated (light, medium, and dark roast) and decaffeinated instant coffee samples inacetylcholinesterase (AchE) inhibition and antioxidant assays, as well as in animal models of Parkinson’s disease. Caffeinatedcoffees inhibited the AchE in much smaller concentrations than decaffeinated coffee. All coffee samples showed antioxidantcapacity without relation with the caffeine content. Blockade in the haloperidol-induced catalepsy was observed with caffeinatedcoffee, but not in the decaffeinated sample. The medium-roast coffee reduced the number of rotations of rats aftermethamphetamine administration on the 6-hydroxydopamine unilateral lesion of the medial forebrain bundle. However, thecoffee treatment did not avoid the loss of dopaminergic neurons on substantia nigra pars compact and only the smallest dose ofcoffee was able to avoid the decrease of dopamine levels in the lesioned side of the striatum. Altogether, these results suggestthat coffee exerts moderate pro-cholinergic and pro-dopaminergic effects and caffeine seems to be the main factor responsiblefor these effects.