EVIDENCE ON THE NEUROPROTECTIVE ROLE OF CAFFEINE IN PARKINSON'S DISEASE: AN INTEGRATIVE REVIEW

Abstract

The increasing prevalence of Parkinson’s disease (PD) has driven the investigation of modifiable risk factors and strategies with neuroprotective potential, with caffeine standing out. This compound acts as an antagonist of adenosine A₂A receptors, present in brain regions related to motor control, such as the basal ganglia. This study aimed to critically analyze the evidence on the relationship between caffeine consumption and PD, exploring its possible neuroprotective effects and clinical implications. This is an integrative review with a qualitative and descriptive approach, conducted between December 2025 and March 2026, based on epidemiological, clinical, and experimental studies. The findings indicate a consistent inverse association between caffeine consumption and the risk of developing PD, often showing a dose-dependent pattern, especially in observational studies. Experimental evidence suggests antioxidant, anti-inflammatory, and mitochondrial function–modulating properties, as well as effects on mechanisms related to α-synuclein accumulation. However, randomized clinical trials show heterogeneous results, with no robust evidence of benefits in disease progression or long-term motor outcomes. Thus, although associated with reduced risk, caffeine has not yet been established as a disease-modifying agent, reinforcing the need for further long-term clinical studies.