PMID- 21919190
OWN - NLM
STAT- MEDLINE
DCOM- 20120214
LR  - 20200930
IS  - 1552-485X (Electronic)
IS  - 1552-4841 (Linking)
VI  - 156B
IP  - 8
DP  - 2011 Dec
TI  - Association of GRIN1 and GRIN2A-D with schizophrenia and genetic interaction with 
      maternal herpes simplex virus-2 infection affecting disease risk.
PG  - 913-22
LID - 10.1002/ajmg.b.31234 [doi]
AB  - N-methyl-D-aspartate (NMDA) receptors are very important for proper brain 
      development and several lines of evidence support that hypofunction of the NMDA 
      receptors are involved in the pathophysiology of schizophrenia. Gene variation 
      and gene-environmental interactions involving the genes encoding the NMDA 
      receptors are therefore likely to influence the risk of schizophrenia. The aim of 
      this study was to determine (1) whether SNP variation in the genes (GRIN1, 
      GRIN2A, GRIN2B, GRIN2C, and GRIN2D) encoding the NMDA receptor were associated 
      with schizophrenia; (2) whether GRIN gene variation in the offspring interacted 
      with maternal herpes simplex virus-2 (HSV-2) seropositivity during pregnancy 
      influencing the risk of schizophrenia later in life. Individuals from three 
      independently collected Danish case control samples were genotyped for 81 tagSNPs 
      (in total 984 individuals diagnosed with schizophrenia and 1,500 control persons) 
      and antibodies against maternal HSV-2 infection were measured in one of the 
      samples (365 cases and 365 controls). Nine SNPs out of 30 in GRIN2B were 
      significantly associated with schizophrenia. One SNP remained significant after 
      Bonferroni correction (rs1806194, P(nominal)  = 0.0008). Significant interaction 
      between maternal HSV-2 seropositivity and GRIN2B genetic variation in the 
      offspring were observed for seven SNPs and two remained significant after 
      Bonferroni correction (rs1805539, P(nominal)  = 0.0001 and rs1806205, P(nominal) 
       = 0.0008). The significant associations and interactions were located at the 3' 
      region of GRIN2B suggesting that genetic variation in this part of the gene may 
      be involved in the pathophysiology of schizophrenia.
CI  - Copyright (c) 2011 Wiley Periodicals, Inc.
FAU - Demontis, Ditte
AU  - Demontis D
AD  - Department of Human Genetics, Aarhus University, Aarhus, Denmark. 
      ditte@humgen.au.dk
FAU - Nyegaard, Mette
AU  - Nyegaard M
FAU - Buttenschon, Henriette N
AU  - Buttenschon HN
FAU - Hedemand, Anne
AU  - Hedemand A
FAU - Pedersen, Carsten B
AU  - Pedersen CB
FAU - Grove, Jakob
AU  - Grove J
FAU - Flint, Tracey J
AU  - Flint TJ
FAU - Nordentoft, Merete
AU  - Nordentoft M
FAU - Werge, Thomas
AU  - Werge T
FAU - Hougaard, David M
AU  - Hougaard DM
FAU - Sorensen, Karina M
AU  - Sorensen KM
FAU - Yolken, Robert H
AU  - Yolken RH
FAU - Mors, Ole
AU  - Mors O
FAU - Borglum, Anders D
AU  - Borglum AD
FAU - Mortensen, Preben Bo
AU  - Mortensen PB
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20110914
PL  - United States
TA  - Am J Med Genet B Neuropsychiatr Genet
JT  - American journal of medical genetics. Part B, Neuropsychiatric genetics : the 
      official publication of the International Society of Psychiatric Genetics
JID - 101235742
RN  - 0 (Carrier Proteins)
RN  - 0 (GRIN1 protein, human)
RN  - 0 (NR2B NMDA receptor)
RN  - 0 (Nerve Tissue Proteins)
RN  - 0 (Receptors, N-Methyl-D-Aspartate)
RN  - VH92ICR8HX (N-methyl D-aspartate receptor subtype 2A)
SB  - IM
MH  - Carrier Proteins/*genetics
MH  - Case-Control Studies
MH  - Female
MH  - Gene Frequency
MH  - *Gene-Environment Interaction
MH  - Genetic Association Studies
MH  - Genetic Predisposition to Disease
MH  - Genetic Variation
MH  - Genotype
MH  - *Herpes Simplex
MH  - Herpesvirus 2, Human/*immunology
MH  - Humans
MH  - Male
MH  - Nerve Tissue Proteins/*genetics
MH  - Polymorphism, Single Nucleotide
MH  - Pregnancy
MH  - *Pregnancy Complications, Infectious
MH  - Receptors, N-Methyl-D-Aspartate/*genetics
MH  - Risk Factors
MH  - Schizophrenia/*genetics
EDAT- 2011/09/16 06:00
MHDA- 2012/02/15 06:00
CRDT- 2011/09/16 06:00
PHST- 2011/01/27 00:00 [received]
PHST- 2011/08/04 00:00 [accepted]
PHST- 2011/09/16 06:00 [entrez]
PHST- 2011/09/16 06:00 [pubmed]
PHST- 2012/02/15 06:00 [medline]
AID - 10.1002/ajmg.b.31234 [doi]
PST - ppublish
SO  - Am J Med Genet B Neuropsychiatr Genet. 2011 Dec;156B(8):913-22. doi: 
      10.1002/ajmg.b.31234. Epub 2011 Sep 14.