FROM NEUROLOGY
Low serum caffeine and caffeine metabolite levels after an overnight fast may be a sensitive way to detect the presence of Parkinson’s disease, according to the results of a new case-control study.
Levels of caffeine and its metabolites were also lower in Parkinson’s disease (PD) patients who had motor dysfunction, compared with those without motor dysfunction, but no differences in serum levels of caffeine metabolites could be detected between patients with mild to more severe stages of PD, reported Motoki Fujimaki, MD, of Juntendo University, Tokyo, and colleagues. The report was published online Jan. 3 in Neurology .
Previous research had shown that people drinking four or more cups of coffee per day had greater than fivefold reduction in risk of developing PD, and mouse models of PD showed that caffeine and two of its metabolites have a neuroprotective effect. Those results suggested that serum caffeine may be useful as a blood marker for PD.
To test that idea, Dr. Fujimaki and associates recruited 31 healthy controls (18 women) and 108 patients with PD but no dementia (50 women). The control group’s mean caffeine intake of 115.81 mg/day (standard deviation, 69.22) was similar to PD patients’ intake of 107.50 mg/day (SD, 67.27).
Serum caffeine levels measured after an overnight fast showed that a cutoff of 33.04 pmol/10 mcL identified PD with an area under the curve (AUC) of 0.78 (sensitivity 76.9%, specificity 74.2%). Inclusion of the primary caffeine metabolites theophylline, theobromine, and paraxanthine improved the AUC to 0.87. When the researchers included all 11 measurable metabolites, the AUC jumped to 0.98.
Genetic analyses found no significant differences in the frequencies of caffeine metabolism–associated genetic variants between PD patients and controls.
The study was limited by the fact that it was conducted at a single university hospital, and the patient population did not include many severe cases. The algorithm should also be studied in other PD patient populations.
The study was funded by grants from several Japanese government agencies. Some of the authors have financial relationships with the pharmaceutical industry.
SOURCE: Fujimaki M et al. Neurology. 2018 Jan 3. doi: 10.1212/WNL.0000000000004888
