Low levels of blood caffeine and its metabolites may help identify patients with early Parkinson’s disease, according to new research. The findings are consistent with caffeine’s neuroprotective effects, previously observed in neurodegenerative diseases.
The study, “Serum caffeine and metabolites are reliable biomarkers of early Parkinson disease,” was published in the journal Neurology. The work was conducted by researchers at the Juntendo University School of Medicine in Tokyo, Japan.
A large number of epidemiological studies report a dose-responsive, inverse relationship between coffee/caffeine consumption and the risk of developing Parkinson’s. However, little is known about caffeine metabolism in Parkinson’s patients.
With that in mind, the team recruited 108 Parkinson’s patients without memory problems plus 31 age-matched healthy people as controls, and investigated their blood caffeine (and 11 of its metabolites) levels and whether there were mutations in their caffeine-related genes.
Both groups consumed the same amount of caffeine (about two cups of coffee a day).
Results showed that even early-onset Parkinson’s patients had significantly lower levels of caffeine and nine of its metabolites in their blood, compared to the control group. This was found to be unrelated to total caffeine intake or the severity of the disease.
“If these results can be confirmed, they would point to an easy test for early diagnosis of Parkinson’s, possibly even before symptoms are appearing. This is important because Parkinson’s disease is difficult to diagnose, especially at the early stages,” David G. Munoz, MD, of the University of Toronto in Canada, who wrote an editorial accompanying the study, said in a news release.
A statistical analysis revealed that this simple blood test was able to reliably identify Parkinson’s patients.
“Likewise, caffeine concentrations in patients with [Parkinson’s disease] with motor complications were significantly decreased compared with those without motor complications,” the team wrote.
When looking at the caffeine-associated genes, researchers reported no differences between Parkinson’s patients and healthy subjects.
Despite the promising results, this is a relative small study which needs to be replicated at a larger scale.
As part of the study’s limitations, people with severe Parkinson’s were not included, making it difficult to detect a relationship between disease severity and blood caffeine levels. Also, all Parkinson’s patients were medicated for the disease, which could influence caffeine metabolism, and thus the study results.
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