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Originally published as Genetics Published Articles Ahead of Print on December 18, 2006.
Genetics, Vol. 175, 917-922, February 2007, Copyright © 2007
doi:10.1534/genetics.106.061796
G72/G30 Genes and Schizophrenia: A Systematic Meta-analysis of Association Studies
Dawei Li*,
,
,1 and
Lin He,
* Bio-X Center, Shanghai Jiao Tong University, Shanghai 200030, China, Institute for Nutritional Sciences, Shanghai Institutes of Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China, Laboratory of Statistical Genetics, Rockefeller University, New York, New York 10021 and NHGG Bio-X Center, Shanghai Jiao Tong University, Shanghai 200030, China
1 Corresponding author: Shanghai Jiao Tong University, Bio-X Center, Hao Ran Bldg., 1954 Hua Shan Rd., Shanghai 200030, China.
E-mail: dwlidwli{at}gmail.com
Schizophrenia may result from a neurotransmission hypofunction of glutamatergic and N-methyl-D-aspartate (NMDA) receptors. Linkage disequilibrium mapping has identified several promising and novel positional candidates, including the G72/G30 and D-amino-acid oxidase (DAAO) genes. Since the first positive association report, many subsequent studies have attempted to replicate the association but the results have been mixed. To try to resolve this inconsistency and to elucidate the relationship between the important glutamate-related genes and schizophrenia, the current meta-analysis has combined samples involving 16 polymorphisms covering all published case-control and family-based association studies up to October 2005. The results suggest that there is weak evidence of association between the G72/G30 genes and schizophrenia.
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