Researchers from the Duke-NUS Graduate Medical School in Singapore have observed that caffeine intake may lower the risk of developing Parkinson’s disease among individuals who carry certain variations of the LRRK2 gene. The study results were published in a prominent medical journal.
The study involved 4488 participants who provided information on their health histories and family medical backgrounds. Volunteers also reported their consumption of coffee and tea, which allowed researchers to assess caffeine exposure alongside genetic risk factors.
Blood samples were collected from all participants to perform genotyping and identify specific LRRK2 variants. Mutations in LRRK2 are the most common genetic causes linked to inherited forms of Parkinson’s disease. In particular, the study focused on three Asian-associated variants: G2385R, R1628P, and S1647T.
Individuals carrying these LRRK2 variants generally face a higher risk of developing Parkinson’s disease, with estimates ranging from one and a half to two times greater than non-carriers. The analysis revealed that caffeine consumption was associated with a significantly reduced risk of Parkinson’s disease among participants who carried the G2385R, R1628P, or S1647T variants.
One likely mechanism is that caffeine blocks adenosine A2A receptors. These receptors are widely present throughout the body, including the nervous system and the cardiovascular system. Changes in the number or activity of adenosine receptors can influence inflammatory processes that accompany many neurological conditions, including Parkinson’s disease. By inhibiting these receptors on the G2385R, R1628P, and S1647T carriers, caffeine may help lessen neuroinflammation linked to the disease.
These findings align with broader observations that caffeine and adenosine receptor antagonism might modulate pathways associated with Parkinson’s. While the results are encouraging, researchers emphasize that caffeine is not a guaranteed preventive measure, and lifestyle and genetic factors interact in complex ways to shape individual risk profiles. Ongoing studies aim to clarify how caffeine affects brain networks involved in motor control and how these effects may differ across diverse populations.
In summary, caffeine consumption appears to be associated with a reduced risk of Parkinson’s disease among people with certain LRRK2 gene variants, notably G2385R, R1628P, and S1647T. The proposed mechanism involves the blockade of adenosine A2A receptors, which can dampen inflammatory processes in the brain. These insights contribute to a growing body of work examining how genetic background and dietary factors intersect to influence neurological health.