No genetic association between postsynaptic density-95 gene polymorphisms and schizophrenia.
Disturbed glutamatergic neurotransmission, especially disturbed N-methyl-D-aspartate (NMDA) receptor function, has been hypothesized to be involved in the pathophysiology of schizophrenia. It may also involve abnormalities in the intracellular signaling machineries that are linked to the NMDA receptor. Postsynaptic density-95 is known to bind NMDA receptor subunits and is involved in intracellular signal transduction and synaptic plasticity. Recently, we reported that gene expression of postsynaptic density-95 was altered in schizophrenic brains compared to controls. Therefore, in this study, we examined six polymorphisms in and around the postsynaptic density-95 gene in 259 schizophrenic cases and 188 healthy controls using TaqMan technology. The results suggested that these six polymorphisms did not affect risk for schizophrenia.
Kawashima
Ritsuko
R
Department of Psychiatry, Juntendo University School of Medicine, Bunkyo-ku, Tokyo 113-8421, Japan. ritsukok@med.juntendo.ac.jp
Ohnuma
Tohru
T
Shibata
Nobuto
N
Arai
Heii
H
D000328:Adult; D016022:Case-Control Studies; D000076122:Disks Large Homolog 4 Protein; D005260:Female; D006801:Humans; D047908:Intracellular Signaling Peptides and Proteins / Q000235:genetics*; D008297:Male; D008565:Membrane Proteins / Q000235:genetics*; D011110:Polymorphism, Genetic; D012559:Schizophrenia / Q000235:genetics*; D018709:Statistics, Nonparametric
C501444:DLG4 protein, human; D000076122:Disks Large Homolog 4 Protein; D047908:Intracellular Signaling Peptides and Proteins; D008565:Membrane Proteins