Caffeine consumption and Parkinson’s disease: a mini-review of current evidence

In the absence of efficient disease-modifying treatments for Parkinson’s disease (PD), research has focused on identifying potential environmental factors whose modulation may prevent or slow the progression of this neurodegenerative disorder. Compelling epidemiological evidence suggests that caffeine consumption is inversely associated with the risk of developing PD. Further experimental findings demonstrated that caffeine, by particularly targeting adenosine A2A (A2AR) receptors, protected PD animal models against the loss of dopaminergic neurons. The antagonistic action of caffeine on adenosine receptors not only slowed PD-related neurodegeneration, but also improved motor and nonmotor symptoms of PD in animal models. Here, we review the potential action mechanisms by which caffeine might play a role in reducing the risk of PD. We also review current evidence of the benefits of caffeine consumption in motor and nonmotor symptoms of PD. Finally, we point out how these promising findings could lead to the identification of new approaches for effective treatment of PD.