Caffeine interaction with glutamate receptor gene GRIN2A: Parkinson's disease in Swedish population.

A complex interplay between genetic and environmental factors is thought to be involved in the etiology of Parkinson's disease (PD). A recent genome-wide association and interaction study (GWAIS) identified GRIN2A, which encodes an NMDA-glutamate-receptor subunit involved in brain's excita...

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Autores principales:	Naomi Yamada-Fowler, Mats Fredrikson, Peter Söderkvist
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2014
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/907fc8b4c5ff466eb5f49b2e413c43aa
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spelling	oai:doaj.org-article:907fc8b4c5ff466eb5f49b2e413c43aa2021-11-18T08:16:19ZCaffeine interaction with glutamate receptor gene GRIN2A: Parkinson's disease in Swedish population.1932-620310.1371/journal.pone.0099294https://doaj.org/article/907fc8b4c5ff466eb5f49b2e413c43aa2014-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/24915238/?tool=EBIhttps://doaj.org/toc/1932-6203A complex interplay between genetic and environmental factors is thought to be involved in the etiology of Parkinson's disease (PD). A recent genome-wide association and interaction study (GWAIS) identified GRIN2A, which encodes an NMDA-glutamate-receptor subunit involved in brain's 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], p<0.001). 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.Naomi Yamada-FowlerMats FredriksonPeter SöderkvistPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 9, Iss 6, p e99294 (2014)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Naomi Yamada-Fowler Mats Fredrikson Peter Söderkvist Caffeine interaction with glutamate receptor gene GRIN2A: Parkinson's disease in Swedish population.
description	A complex interplay between genetic and environmental factors is thought to be involved in the etiology of Parkinson's disease (PD). A recent genome-wide association and interaction study (GWAIS) identified GRIN2A, which encodes an NMDA-glutamate-receptor subunit involved in brain's 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], p<0.001). 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.
format	article
author	Naomi Yamada-Fowler Mats Fredrikson Peter Söderkvist
author_facet	Naomi Yamada-Fowler Mats Fredrikson Peter Söderkvist
author_sort	Naomi Yamada-Fowler
title	Caffeine interaction with glutamate receptor gene GRIN2A: Parkinson's disease in Swedish population.
title_short	Caffeine interaction with glutamate receptor gene GRIN2A: Parkinson's disease in Swedish population.
title_full	Caffeine interaction with glutamate receptor gene GRIN2A: Parkinson's disease in Swedish population.
title_fullStr	Caffeine interaction with glutamate receptor gene GRIN2A: Parkinson's disease in Swedish population.
title_full_unstemmed	Caffeine interaction with glutamate receptor gene GRIN2A: Parkinson's disease in Swedish population.
title_sort	caffeine interaction with glutamate receptor gene grin2a: parkinson's disease in swedish population.
publisher	Public Library of Science (PLoS)
publishDate	2014
url	https://doaj.org/article/907fc8b4c5ff466eb5f49b2e413c43aa
work_keys_str_mv	AT naomiyamadafowler caffeineinteractionwithglutamatereceptorgenegrin2aparkinsonsdiseaseinswedishpopulation AT matsfredrikson caffeineinteractionwithglutamatereceptorgenegrin2aparkinsonsdiseaseinswedishpopulation AT petersoderkvist caffeineinteractionwithglutamatereceptorgenegrin2aparkinsonsdiseaseinswedishpopulation
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Caffeine interaction with glutamate receptor gene GRIN2A: Parkinson's disease in Swedish population.

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