PMID- 22695185
OWN - NLM
STAT- MEDLINE
DCOM- 20130227
LR  - 20211203
IS  - 1873-2402 (Electronic)
IS  - 0006-3223 (Linking)
VI  - 72
IP  - 8
DP  - 2012 Oct 15
TI  - Brain-derived neurotrophic factor levels and its Val66Met gene polymorphism 
      predict tardive dyskinesia treatment response to Ginkgo biloba.
PG  - 700-6
LID - S0006-3223(12)00418-0 [pii]
LID - 10.1016/j.biopsych.2012.04.032 [doi]
AB  - BACKGROUND: Tardive dyskinesia (TD) has no well-accepted treatments or known 
      pathophysiology, but low brain-derived neurotrophic factor (BDNF) may play an 
      important role in its pathophysiology. Ginkgo biloba (EGb-761) is a potent 
      antioxidant that has neuroprotective effects mediated through enhancing BDNF 
      levels. We hypothesized that treatment with EGb-761 would increase serum BDNF 
      levels and reduce TD, particularly among schizophrenia patients who have the BDNF 
      valine 66 to methionine (Val66Met) genotype (Val/Val). METHODS: Serum BDNF levels 
      and genotyping for the BDNF gene Val66Met polymorphism were assessed in Chinese 
      schizophrenic patients with (n = 368) and without (n = 563) TD as well as healthy 
      control subjects (n = 546). About half of the TD patients (n = 157) then 
      participated in a double-blind, randomized, placebo-control 12-week treatment 
      with 240 mg per day of EGb-761. Serum BDNF levels were measured again at 
      posttreatment. Clinical efficacy was determined using the Abnormal Involuntary 
      Movement Scale (AIMS). RESULTS: TD patients had lower BDNF levels than the non-TD 
      patients and healthy controls. EGb-761 treatment improved symptoms of TD and 
      increased BDNF levels compared with placebo treatment. Moreover, the improvement 
      of AIMS total score correlated with the increase in BDNF levels. Furthermore, 
      improvement in the AIMS score was greatest in those with the Val/Val allele and 
      lowest with the Met/Met allele. CONCLUSIONS: The BDNF system may be implicated in 
      the pathophysiology of TD and its improvement with antioxidant treatment. 
      Furthermore, patients with the genetic potential for greater BDNF release 
      (Val/Val at 66) may obtain a greater reduction in TD from EGb-761 treatment.
CI  - Copyright (c) 2012 Society of Biological Psychiatry. Published by Elsevier Inc. All 
      rights reserved.
FAU - Zhang, Xiang Yang
AU  - Zhang XY
AD  - Menninger Department of Psychiatry and Behavioral Sciences, Baylor College of 
      Medicine, Houston, Texas, USA. xyzhang@bcm.edu
FAU - Zhang, Wu-Fang
AU  - Zhang WF
FAU - Zhou, Dong-Feng
AU  - Zhou DF
FAU - Chen, Da Chun
AU  - Chen DC
FAU - Xiu, Mei Hong
AU  - Xiu MH
FAU - Wu, Hao-Ran
AU  - Wu HR
FAU - Haile, Colin N
AU  - Haile CN
FAU - Kosten, Therese A
AU  - Kosten TA
FAU - Kosten, Thomas R
AU  - Kosten TR
LA  - eng
GR  - P50-DA18827/DA/NIDA NIH HHS/United States
GR  - U01-MH79639/MH/NIMH NIH HHS/United States
PT  - Journal Article
PT  - Randomized Controlled Trial
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
DEP - 20120612
PL  - United States
TA  - Biol Psychiatry
JT  - Biological psychiatry
JID - 0213264
RN  - 0 (Antipsychotic Agents)
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Plant Extracts)
RN  - 19FUJ2C58T (Ginkgo biloba extract)
RN  - AE28F7PNPL (Methionine)
RN  - HG18B9YRS7 (Valine)
SB  - IM
MH  - Adult
MH  - Analysis of Variance
MH  - Antipsychotic Agents/adverse effects
MH  - Brain-Derived Neurotrophic Factor/*blood/*genetics
MH  - China
MH  - Female
MH  - Genotype
MH  - Ginkgo biloba
MH  - Humans
MH  - Male
MH  - Methionine/*genetics
MH  - Middle Aged
MH  - Movement Disorders/blood/*drug therapy/etiology/*genetics
MH  - Pharmacogenetics
MH  - Plant Extracts/*therapeutic use
MH  - Polymorphism, Genetic/*genetics
MH  - Predictive Value of Tests
MH  - Regression Analysis
MH  - Schizophrenia/drug therapy
MH  - Severity of Illness Index
MH  - Treatment Outcome
MH  - Valine/*genetics
EDAT- 2012/06/15 06:00
MHDA- 2013/02/28 06:00
CRDT- 2012/06/15 06:00
PHST- 2012/01/24 00:00 [received]
PHST- 2012/04/25 00:00 [revised]
PHST- 2012/04/26 00:00 [accepted]
PHST- 2012/06/15 06:00 [entrez]
PHST- 2012/06/15 06:00 [pubmed]
PHST- 2013/02/28 06:00 [medline]
AID - S0006-3223(12)00418-0 [pii]
AID - 10.1016/j.biopsych.2012.04.032 [doi]
PST - ppublish
SO  - Biol Psychiatry. 2012 Oct 15;72(8):700-6. doi: 10.1016/j.biopsych.2012.04.032. 
      Epub 2012 Jun 12.