<?xml version="1.0" encoding="UTF-8"?><xml><records><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Liu, Hsin-Ping</style></author><author><style face="normal" font="default" size="100%">Lin, Wei-Yong</style></author><author><style face="normal" font="default" size="100%">Liu, Shu-Hsiang</style></author><author><style face="normal" font="default" size="100%">Wang, Wen-Fu</style></author><author><style face="normal" font="default" size="100%">Tsai, Chon-Haw</style></author><author><style face="normal" font="default" size="100%">Wu, Bor-Tsang</style></author><author><style face="normal" font="default" size="100%">Wang, Chien-Kuo</style></author><author><style face="normal" font="default" size="100%">Tsai, Fuu-Jen</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Genetic variation in N-methyl-D-aspartate receptor subunit NR3A but not NR3B influences susceptibility to Alzheimer&#039;s disease.</style></title><secondary-title><style face="normal" font="default" size="100%">Dement Geriatr Cogn Disord</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Dement Geriatr Cogn Disord</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Aged</style></keyword><keyword><style  face="normal" font="default" size="100%">Alleles</style></keyword><keyword><style  face="normal" font="default" size="100%">Alzheimer Disease</style></keyword><keyword><style  face="normal" font="default" size="100%">DNA</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Genetic Markers</style></keyword><keyword><style  face="normal" font="default" size="100%">Genetic Predisposition to Disease</style></keyword><keyword><style  face="normal" font="default" size="100%">Genotype</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Middle Aged</style></keyword><keyword><style  face="normal" font="default" size="100%">Odds Ratio</style></keyword><keyword><style  face="normal" font="default" size="100%">Polymorphism, Single Nucleotide</style></keyword><keyword><style  face="normal" font="default" size="100%">Receptors, N-Methyl-D-Aspartate</style></keyword><keyword><style  face="normal" font="default" size="100%">Risk Factors</style></keyword><keyword><style  face="normal" font="default" size="100%">Taiwan</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2009</style></year></dates><volume><style face="normal" font="default" size="100%">28</style></volume><pages><style face="normal" font="default" size="100%">521-7</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;&lt;b&gt;BACKGROUND: &lt;/b&gt;The administration of memantine, an N-methyl-D-aspartate (NMDA) receptor antagonist, has clinically improved the cognitive function of patients with Alzheimer&#039;s disease (AD), indicating that a disturbance in glutamatergic transmission might be involved in a predisposition to developing the disease.&lt;/p&gt;

&lt;p&gt;&lt;b&gt;AIM: &lt;/b&gt;The potential association of polymorphisms in NMDA receptor subunits NR3A and NR3B, encoded by the GRIN3A and GRIN3B genes, with AD was investigated.&lt;/p&gt;

&lt;p&gt;&lt;b&gt;METHODS: &lt;/b&gt;We performed a case-control study. Two single nucleotide polymorphisms, 3104 G/A (rs10989563) and 3723 G/A (rs3739722), in the GRIN3A gene and 2 GRIN3B gene polymorphisms, 1210 C/T (rs4807399) and 1730 C/T (rs2240158), were studied.&lt;/p&gt;

&lt;p&gt;&lt;b&gt;RESULTS: &lt;/b&gt;Upon genotyping of the exonic polymorphism in the GRIN3A gene, the G allele was present at a higher rate than the A allele at position 3723 in AD patients compared with normal groups (p &amp;lt; 0.05). Three haplotypes (designated Ht1-3) were identified from these 2 polymorphisms (3104 G/A and 3723 G/A), and the distribution of Ht2 (AG) differed between AD patients and controls (p &amp;lt; 0.05). Additionally, from the 2 GRIN3B gene variants 1210 C/T and 1730 C/T analyzed, no strong association with AD was observed.&lt;/p&gt;

&lt;p&gt;&lt;b&gt;CONCLUSION: &lt;/b&gt;These observations suggest that the genetic variation of the NR3A, but not NR3B, subunit of the NMDA receptor may be a risk factor for AD pathogenesis among the Taiwanese population.&lt;/p&gt;
</style></abstract><issue><style face="normal" font="default" size="100%">6</style></issue><custom1><style face="normal" font="default" size="100%">&lt;p&gt;http://www.ncbi.nlm.nih.gov/pubmed/20016182?dopt=Abstract&lt;/p&gt;
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