Abstract
Caffeine is considered to be a neuroprotective agent against Parkinson's disease (PD) and is expected to offer a blood-based biomarker for the disease. We herein investigated the ability of this biomarker to discriminate between PD and neurodegenerative diseases. To quantify caffeine concentrations in serum and plasma, we developed a specific competitive enzyme-linked immunosorbent assay (ELISA). To validate the diagnostic performance of the assay, we conducted a case control-study of two independent cohorts among controls and patients with PD and multiple system atrophy (MSA). Parallelism, recovery rate, and intra- and inter-assay precision of our assay were within the standard of acceptance. In the first cohort of 31 PD patients, 18 MSA patients and 33 age-matched controls, serum caffeine levels were significantly lower in PD patients than in Controls (p = 0.018). A similar trend was also observed in the MSA group, but did not reach the level of significance. In the second cohort of 50 PD patients, 50 MSA patients and 45 age-matched controls, plasma caffeine levels were significantly decreased in both PD and MSA groups compared to Controls (p < 0.001). This originally developed ELISA offered sufficient sensitivity to detect caffeine in human serum and plasma. We reproducibly confirmed decreased blood concentrations of caffeine in PD compared to controls using this ELISA. A similar trend was observed in the MSA group, despite a lack of consistent significant differences across cohorts.
Highlights
Many reports have examined the relationship between Parkinson’s disease (PD) and caffeine in epidemiology, animal experiments, and clinical pharmacology
Mean differences in caffeine between PD, multiple system atrophy (MSA), and Control groups were analyzed by one-way ANOVA and Bonferroni’s multiple comparison test
The originally developed enzyme-linked immunosorbent assay (ELISA) examined in this study offered sufficiently high sensitivity to detect caffeine in human serum and plasma
Summary
Many reports have examined the relationship between Parkinson’s disease (PD) and caffeine in epidemiology, animal experiments, and clinical pharmacology. Recent metabolome analyses have shown that blood levels of caffeine metabolites were significantly lower in PD patients than in healthy subjects, and could be used as a candidate biomarker for predicting progression of PD [7,8,9]. In those reports, plasma caffeine concentration was quantified using mass spectrometry, which is ill-suited to application in clinical practice due to the high running costs. The utility of quantifying caffeine concentration has not been confirmed as useful for discriminating PD from other neurodegenerative diseases, such as multiple system atrophy (MSA)
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