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Published on: February 26, 2012
Interaction between BDNF Val66Met polymorphism and mismatch negativity for working memory capacity in schizophrenia
Wenpeng Hou1,2, Xiangqin Qin1,2, Hang Li1,2
1Beijing Key Laboratory of Mental Disorders, National Clinical Research Center for Mental Disorders & National Center for Mental Disorders, Beijing Anding Hospital, Capital Medical University, Beijing, China.
Brain-derived neurotrophic factor (BDNF) Val homozygotes show improved working memory in schizophrenia. BDNF genotype interacts with mismatch negativity (MMN) for working memory capacity, suggesting a link with N-methyl-D-aspartate receptor function.
Area of Science:
- Neuroscience
- Psychiatry
- Genetics
Background:
- Schizophrenia is associated with working memory impairments.
- Brain-derived neurotrophic factor (BDNF) Val/Met polymorphism and mismatch negativity (MMN) amplitude are linked to these impairments.
- Research exploring the interplay between BDNF genotype, MMN, and working memory in schizophrenia is scarce.
Purpose of the Study:
- To investigate the relationships among BDNF genotype, MMN amplitude, and working memory capacity in schizophrenia patients.
- To explore potential interactions between these factors in the context of transcranial direct current stimulation (tDCS) intervention.
Main Methods:
- Secondary analysis of a randomized, double-blind, controlled trial involving tDCS for working memory enhancement in schizophrenia.
- Assessment of BDNF genotype, MMN amplitude, and working memory capacity at baseline and post-intervention.
- Patients were divided into dorsolateral prefrontal cortex stimulation, posterior parietal cortex stimulation, and sham stimulation groups.
Main Results:
- BDNF Val homozygotes, compared to Met-carriers, had better working memory capacity and fewer symptoms at baseline.
- A significant correlation between MMN amplitude and working memory capacity was observed exclusively in BDNF Val homozygotes.
- In the tDCS group with MMN improvement, BDNF Val homozygotes showed greater working memory enhancement than Met-carriers.
Conclusions:
- This study provides in vivo evidence for an interaction between MMN and BDNF Val/Met polymorphism in influencing working memory capacity in schizophrenia.
- The findings suggest a connection between BDNF, N-methyl-D-aspartate receptor (NMDAR) function (as indicated by MMN), and working memory in schizophrenia.
- BDNF genotype may modulate the effects of interventions targeting MMN for working memory improvement.
