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Caffeine Interaction with Glutamate Receptor Gene GRIN2A: Parkinsons Disease in Swedish Population
Linköping University, Department of Clinical and Experimental Medicine, Division of Cell Biology. Linköping University, Faculty of Health Sciences.
Linköping University, Department of Clinical and Experimental Medicine, Division of Inflammation Medicine. Linköping University, Faculty of Health Sciences.
Linköping University, Department of Clinical and Experimental Medicine, Division of Cell Biology. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Center for Diagnostics, Department of Clinical Pathology and Clinical Genetics.
2014 (English)In: PLoS ONE, ISSN 1932-6203, E-ISSN 1932-6203, Vol. 9, no 6, e99294- p.Article in journal (Refereed) Published
Abstract [en]

A complex interplay between genetic and environmental factors is thought to be involved in the etiology of Parkinsons disease (PD). A recent genome-wide association and interaction study (GWAIS) identified GRIN2A, which encodes an NMDA-glutamate-receptor subunit involved in brains excitatory neurotransmission, as a PD genetic modifier in inverse association with caffeine intake. Here in, we attempted to replicate the reported association of a single nucleotide polymorphism, GRIN2A_rs4998386, and its interaction with caffeine intake with PD in patient-control study in an ethnically homogenous population in southeastern Sweden, as consistent and independent genetic association studies are the gold standard for the validation of genome-wide association studies. All the subjects (193 sporadic PD patients and 377 controls) were genotyped, and the caffeine intake data was obtained by questionnaire. We observed an association between rs4998386 and PD with odds ratio (OR) of 0.61, 95% confidence intervals (CI) of 0.39-0.96, p = 0.03, under a model excluding rare TT allele. There was also a strong significance in joint effects of gene and caffeine on PD risk (TC heavy caffeine vs. CC light caffeine: OR = 0.38, 95% CI = [0.20-0.70], p = 0.002) and gene-caffeine interaction (OR = 0.998, 95% CI = [0.991-0.999], pless than0.001). Overall, our results are in support of the findings of the GWAIS and provided additional evidence indicating PD protective effects of coffee drinking/caffeine intake as well as the interaction with glutamate receptor genotypes.

Place, publisher, year, edition, pages
Public Library of Science , 2014. Vol. 9, no 6, e99294- p.
National Category
Clinical Medicine
Identifiers
URN: urn:nbn:se:liu:diva-110984DOI: 10.1371/journal.pone.0099294ISI: 000340947700080PubMedID: 24915238OAI: oai:DiVA.org:liu-110984DiVA: diva2:751588
Note

Funding Agencies|Foundation for Parkinsons Research at Linkoping University, Sweden (Stiftelsen for Parkinsonforskning) [20110525]

Available from: 2014-10-01 Created: 2014-10-01 Last updated: 2017-12-05

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Yamada, NaomiFredrikson, MatsSöderkvist, Peter

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