Genetic study of eight AKT1 gene polymorphisms and their interaction with DRD2 gene polymorphisms in tardive dyskinesia.
Tardive dyskinesia (TD) is a motor adverse effect of chronic antipsychotic medication. It has been suggested to involve dopamine neurotransmission system changes. AKT1 acts downstream of the D(2) receptor that is blocked by all antipsychotics to some degree. The AKT1 gene has not been investigated in TD. We examined eight polymorphisms spanning the AKT1 gene and their association with TD in our schizophrenia sample of 193 Caucasians, 76 of which with TD. AKT1 polymorphisms and haplotypes were not significantly associated with TD. However, we detected a significant interaction between rs6275 of DRD2 and rs3730358 of AKT1 (p<1 x 10(-5)).
Zai
Clement C
CC
Centre for Addiction and Mental Health, Toronto, Ontario, Canada.
Romano-Silva
Marco A
MA
Hwang
Rudi
R
Zai
Gwyneth C
GC
Deluca
Vincenzo
V
Müller
Daniel J
DJ
King
Nicole
N
Voineskos
Aristotle N
AN
Meltzer
Herbert Y
HY
Lieberman
Jeffrey A
JA
Potkin
Steven G
SG
Remington
Gary
G
Kennedy
James L
JL
D000328:Adult; D001741:Black or African American / Q000235:genetics; D014150:Antipsychotic Agents / Q000009:adverse effects*; D004409:Dyskinesia, Drug-Induced / Q000209:etiology / Q000235:genetics*; D005260:Female; D005787:Gene Frequency; D055106:Genome-Wide Association Study; D005838:Genotype; D006801:Humans; D008297:Male; D011110:Polymorphism, Genetic; D051057:Proto-Oncogene Proteins c-akt / Q000235:genetics*; D017448:Receptors, Dopamine D2 / Q000235:genetics*; D012559:Schizophrenia / Q000188:drug therapy* / Q000235:genetics; D044465:White People / Q000235:genetics
D014150:Antipsychotic Agents; D017448:Receptors, Dopamine D2; C494918:AKT1 protein, human; D051057:Proto-Oncogene Proteins c-akt