Interaction between BDNF Val66Met polymorphism and mismatch negativity for working memory capacity in schizophrenia.

IF 3 Q2 PSYCHIATRY
Wenpeng Hou, Xiangqin Qin, Hang Li, Qi Wang, Yushen Ding, Xiongying Chen, Ru Wang, Fang Dong, Qijing Bo, Xianbin Li, Fuchun Zhou, Chuanyue Wang
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Abstract

Both the brain-derived neurotrophic factor (BDNF) valine (Val)/methionine (Met) polymorphism and mismatch negativity (MMN) amplitude are reportedly linked to working memory impairments in schizophrenia. However, there is evident scarcity of research aimed at exploring the relationships among the three factors. In this secondary analysis of a randomized, controlled, double-blind trial, we investigated these relationships. The trial assessed the efficacy of transcranial direct current stimulation for enhancing working memory in clinically stable schizophrenia patients, who were randomly divided into three groups: dorsolateral prefrontal cortex stimulation, posterior parietal cortex stimulation, and sham stimulation groups. Transcranial direct current stimulation was administered concurrently with a working memory task over five days. We assessed the BDNF genotype, MMN amplitude, working memory capacity, and interference control subdomains. These assessments were conducted at baseline with 54 patients and followed up post-intervention with 48 patients. Compared to BDNF Met-carriers, Val homozygotes exhibited fewer positive and general symptoms and increased working memory capacity at baseline. A correlation between MMN amplitude and working memory capacity was noted only in BDNF Val homozygotes. The correlations were significantly different in the two BDNF genotype groups. Furthermore, in the intervention group that showed significant improvement in MMN amplitude, BDNF Val homozygotes exhibited greater enhancement in working memory capacity than Met-carriers. This study provides in vivo evidence for the interaction between MMN and BDNF Val/Met polymorphism for working memory capacity. As MMN has been considered a biomarker of N-methyl-D-aspartate receptor (NMDAR) function, these data shed light on the complex interactions between BDNF and NMDAR in terms of working memory in schizophrenia.

Abstract Image

BDNF Val66Met多态性与错配负性对精神分裂症工作记忆能力的相互作用
据报道,脑源性神经营养因子(BDNF)缬氨酸(Val)/蛋氨酸(Met)多态性和错配负性(MMN)振幅都与精神分裂症患者的工作记忆障碍有关。然而,旨在探索这三个因素之间关系的研究明显不足。在这项随机对照双盲试验的二次分析中,我们对这些关系进行了调查。该试验评估了经颅直流电刺激对临床稳定的精神分裂症患者增强工作记忆的疗效,这些患者被随机分为三组:背外侧前额叶皮层刺激组、后顶叶皮层刺激组和假刺激组。经颅直流电刺激与工作记忆任务同时进行,为期五天。我们对 BDNF 基因型、MMN 振幅、工作记忆能力和干扰控制子域进行了评估。54名患者接受了基线评估,48名患者接受了干预后随访。与BDNF Met携带者相比,Val同卵双生者在基线时表现出较少的积极症状和一般症状,工作记忆能力也有所提高。只有 BDNF Val 基因同型携带者的 MMN 振幅与工作记忆能力之间存在相关性。两个 BDNF 基因型组的相关性存在明显差异。此外,在MMN振幅有明显改善的干预组中,BDNF Val同型基因携带者的工作记忆能力比Met基因携带者有更大的提高。这项研究为 MMN 与 BDNF Val/Met 多态性在工作记忆能力方面的相互作用提供了体内证据。由于 MMN 被认为是 N-甲基-D-天冬氨酸受体(NMDAR)功能的生物标志物,这些数据揭示了 BDNF 和 NMDAR 在精神分裂症患者工作记忆方面的复杂相互作用。
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