Potential implications of caffeine effects for adenosine neuromodulation
Parkinson’s disease
The absence of the classic psychostimulation of caffeine and the impaired attention in caffeine withdrawal, as indexed by the performance in 0-back, corroborate earlier results in a psychomotor vigilance taskFurthermore, ample in vitro evidence shows that, in contrast to the propensity of A1R in developing tolerance to caffeine, A2AR properties and the behavioral effects of A2AR antagonism are rather resistant over daily caffeine intakeThe resistance of A2AR antagonism may further explain the reduced hippocampal activity during daily caffeine intake. Caffeine intake was found to reduce hippocampal long-term potentiation (LTP), a marker of synaptic plasticity, in freely behaving rodentsNotably, there is evidence in non-caffeine consumers that decaffeinated espresso can impede the increase in cortical excitability triggered by a transcranial alternating current stimulation in a placebo conditionThe predominance of A2AR antagonism underlying the effects of daily caffeine intake might also serve as a neurobiological fundament of the divergent impacts of caffeine on healthy versus clinical populations. Chronic caffeine administration has been frequently reported to exert beneficial effects under conditions involving an A2AR overexpression, including Parkinson’s disease