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Caffeine, creatine, GRIN2A and Parkinson's disease progression
David K Simon1, Cai Wu2, Barbara C Tilley2
1Department of Neurology, Beth Israel Deaconess Medical Center, Harvard Medical School, 330 Brookline Avenue, Boston, MA 02215, USA.
Journal of the Neurological Sciences
|March 22, 2017
Summary
Caffeine and creatine may interact to worsen Parkinson's disease (PD) progression, especially in individuals with a specific GRIN2A gene variant. This highlights complex gene-environment interactions in PD.
Area of Science:
- Neuroscience
- Genetics
- Pharmacology
Background:
- Caffeine shows neuroprotective effects in Parkinson's disease (PD) animal models and is inversely associated with PD risk in humans.
- The GRIN2A gene, encoding an NMDA-glutamate-receptor subunit, may influence the association between caffeine and PD.
- Previous studies found no link between caffeine intake and PD progression, except in creatine users where higher caffeine intake correlated with faster progression.
Purpose of the Study:
- To investigate the complex interactions between caffeine, creatine, GRIN2A genotype, and Parkinson's disease (PD) progression.
- To analyze data from 420 subjects in a placebo-controlled creatine study for PD, examining DNA samples and caffeine intake.
Main Methods:
- Analysis of data from 420 Parkinson's disease (PD) patients from a placebo-controlled creatine study.
- Assessment of GRIN2A genotype, caffeine intake, creatine use, and clinical progression rates over time.
- Statistical analysis to identify interactions between these factors.
Main Results:
- No association was found between GRIN2A genotype and PD progression in the placebo group.
- A significant four-way interaction was observed between GRIN2A genotype, caffeine, creatine, and time since baseline.
- In the creatine group, high caffeine intake combined with the GRIN2A T allele was associated with more rapid PD progression (p=0.03).
Conclusions:
- The detrimental interaction between caffeine and creatine on PD progression is influenced by GRIN2A genotype.
- This finding exemplifies the intricate nature of gene-environment interactions in Parkinson's disease progression.
- Further research is needed to elucidate the mechanisms underlying these complex interactions.
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