Objective: To investigate the relationship between dietary caffeine intake and striatal dopamine function over the progression of Parkinson’s disease (PD).

Background: The association between high caffeine consumption and the reduced risk for PD has been replicated in several epidemiological studies. However, there is limited evidence of the effects of caffeine on disease progression in already diagnosed patients with PD. We performed a two-part neuroimaging study to uncover the effects of high and low dietary caffeine intake on brain dopamine transporter (DAT) binding.

Method: Part I Cross-sectional: 115 early unmedicated PD patients (mean age=64.3 years, 46% men) and 40 healthy controls were investigated. Each subject was scanned with [¹²³I]FP-CIT SPECT and striatal DAT-binding was evaluated using specific binding ratios (SBRs) in association with the level of daily coffee consumption (low: 0-3 cups/day, high: > 3 cups/day).

Part II Longitudinal: 44 PD patients out of Part I were scanned again with a mean interval of 5.5 years. Caffeine consumption over the study period was investigated with the Caffeine Consumption Questionnaire-Revised (CCQ-R) and ANCOVA was used in association with yearly progressive striatal DAT-binding loss.

Results: Part I: PD patients with high coffee consumption (n=58), had 8.3-15.4% lower DAT binding in all studied striatal regions compared to patients with low consumption (n=57) after controlling for the effects of age, sex and MDS-UPDRS motor score (e.g. left putamen: F(1,109)=8.26, p=0.005; right caudate: F(1,109)=9.76, p=0.002). No similar effects were seen in healthy controls.

Part II: Higher caffeine consumption was associated with a greater reduction in striatal DAT binding. In PD patients unmedicated at baseline (n=29), the effect was seen in left and right putamen and left caudate when controlling for age, sex and change in MDS-UPDRS motor score (e.g. right putamen: F(1,24)=7.83, p=0.010).

Conclusion: PD patients with high caffeine consumption have lower striatal DAT binding compared to patients with low consumption. This difference progressively increases during the course of PD. Considering the protective effect of caffeine in epidemiological studies, the observed effect could reflect a compensatory decrease in DAT surface expression in PD due to adenosine-dopamine receptor interaction and caffeine-induced increased dopamine release.

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MDS Abstracts - https://www.mdsabstracts.org/abstract/effect-of-dietary-caffeine-on-brain-dopamine-transporter-binding-in-parkinsons-disease/