PMID- 19457211
OWN - NLM
STAT- MEDLINE
DCOM- 20091013
LR  - 20221207
IS  - 1440-1819 (Electronic)
IS  - 1323-1316 (Linking)
VI  - 63
IP  - 4
DP  - 2009 Aug
TI  - Genetic association of BDNF val66met and GSK-3beta-50T/C polymorphisms with 
      tardive dyskinesia.
PG  - 433-9
LID - 10.1111/j.1440-1819.2009.01976.x [doi]
AB  - AIMS: Neurodegenerative processes may be involved in the pathogenesis of tardive 
      dyskinesia (TD), and a growing body of evidence suggests that brain-derived 
      neurotrophic factor (BDNF) plays a role in both the antipsychotic effects and the 
      pathogenesis of TD. BDNF and glycogen synthase kinase (GSK)-3beta are important 
      in neuronal survival, and thus abnormal regulation of BDNF and GSK-3beta may 
      contribute to TD pathophysiology. This study investigated the relationship 
      between two polymorphisms, val66met in the BDNF coding region and -50T/C in the 
      GSK-3beta promoter, and susceptibility to TD among a matched sample of patients 
      having schizophrenia with TD (n = 83), patients with schizophrenia without TD (n 
      = 78), and normal control subjects (n = 93). METHODS: All subjects were Korean. 
      The BDNF val66met and GSK-3beta-50T/C genotypes were determined by polymerase 
      chain reaction and restriction fragment length polymorphism analyses. RESULTS: 
      Polymerase chain reaction analysis revealed no significant difference in the 
      occurrence of the polymorphisms among the TD, non-TD, and control subjects, but a 
      significant interaction was observed among the groups possessing BDNF val allele 
      in compound genotypes (P = 0.001). We found that the schizophrenic subjects with 
      the C/C GSK-3beta genotype, who carry the val allele of the BDNF gene, are 
      expected to have a decreased risk of developing neuroleptic-induced tardive 
      dyskinesia (P < 0.001). CONCLUSIONS: Our results demonstrate that the GSK-3beta 
      C/C genotype with the BDNF val allele is associated with patients having 
      schizophrenia without TD. This study also suggests that the BDNF and GSK-3beta 
      gene polymorphisms work in combination, but not individually, in predisposing 
      patients with schizophrenia to TD.
FAU - Park, Sung Woo
AU  - Park SW
AD  - Paik Institute for Clinical Research, Inje University, Busan, Republic of Korea.
FAU - Lee, Jung Goo
AU  - Lee JG
FAU - Kong, Bo Geum
AU  - Kong BG
FAU - Lee, Sun Jung
AU  - Lee SJ
FAU - Lee, Chan Hong
AU  - Lee CH
FAU - Kim, Jeong Ik
AU  - Kim JI
FAU - Kim, Young Hoon
AU  - Kim YH
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20090427
PL  - Australia
TA  - Psychiatry Clin Neurosci
JT  - Psychiatry and clinical neurosciences
JID - 9513551
RN  - 0 (Antipsychotic Agents)
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - AE28F7PNPL (Methionine)
RN  - EC 2.7.11.1 (GSK3B protein, human)
RN  - EC 2.7.11.1 (Glycogen Synthase Kinase 3 beta)
RN  - EC 2.7.11.26 (Glycogen Synthase Kinase 3)
RN  - HG18B9YRS7 (Valine)
SB  - IM
MH  - Adult
MH  - Alleles
MH  - Antipsychotic Agents/*adverse effects/therapeutic use
MH  - Asian People/genetics
MH  - Brain-Derived Neurotrophic Factor/*genetics
MH  - Dyskinesia, Drug-Induced/etiology/*genetics
MH  - Female
MH  - Gene Frequency
MH  - Genetic Predisposition to Disease
MH  - Genetic Variation
MH  - Genome-Wide Association Study
MH  - Genotype
MH  - Glycogen Synthase Kinase 3/*genetics
MH  - Glycogen Synthase Kinase 3 beta
MH  - Humans
MH  - Korea
MH  - Male
MH  - Methionine/genetics
MH  - Polymerase Chain Reaction
MH  - *Polymorphism, Genetic
MH  - Schizophrenia/*drug therapy/genetics
MH  - Valine/genetics
EDAT- 2009/05/22 09:00
MHDA- 2009/10/14 06:00
CRDT- 2009/05/22 09:00
PHST- 2009/05/22 09:00 [entrez]
PHST- 2009/05/22 09:00 [pubmed]
PHST- 2009/10/14 06:00 [medline]
AID - PCN1976 [pii]
AID - 10.1111/j.1440-1819.2009.01976.x [doi]
PST - ppublish
SO  - Psychiatry Clin Neurosci. 2009 Aug;63(4):433-9. doi: 
      10.1111/j.1440-1819.2009.01976.x. Epub 2009 Apr 27.