Is serum brain-derived neurotrophic factor a biomarker for cognitive enhancement in schizophrenia?
Is serum brain-derived neurotrophic factor a biomarker for cognitive enhancement in schizophrenia?
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DOI：
10.1016/j.biopsych.2009.02.017
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发表时间：
2009-09-15
影响因子：
10.6
通讯作者：
Mellon SH
中科院分区：
文献类型：
--
作者：
Vinogradov S;Fisher M;Holland C;Shelly W;Wolkowitz O;Mellon SH
脑源性神经营养因子（BDNF）在神经发育和可塑性中起关键作用; BDNF功能下降可能有助于精神分裂症的发病机制。然而，BDNF的水平不是静止的;在动物实验中，脑BDNF在空间学习过程中增加，在临床抑郁症中，成功的抗抑郁治疗会提高血清BDNF。我们问：精神分裂症患者基于神经可塑性的认知训练是否会导致血清BDNF增加？对五十六例精神分裂症门诊患者和16例匹配的健康对照者进行了基线认知能力和血清BDNF的评估。精神分裂症受试者被随机分配到50小时（10周）的计算机听觉训练或计算机游戏控制条件下，随后重新评估认知和血清BDNF。在基线时，精神分裂症参与者的血清BDNF显著低于正常水平。与玩电脑游戏的受试者相比，从事旨在改善听觉处理的计算机认知训练的精神分裂症受试者表现出显着的认知增益和血清BDNF显着增加。这种增加在训练2周后明显，在活动状态下10周后，受试者的平均血清BDNF水平“正常化”，而对照组没有变化。在活动状态下，脑源性神经营养因子的变化与生活质量的改善显着相关。临床稳定的慢性精神分裂症患者在接受基于神经可塑性的认知训练后血清BDNF水平显著升高，但在玩电脑游戏后则没有。血清BDNF水平可作为强化认知训练效果的外周生物标志物，并可为评估精神分裂症患者的认知增强方法提供有用的工具。
Brain-derived neurotrophic factor (BDNF) plays a critical role in neurodevelopment and plasticity; decreased BDNF functioning may contribute to the pathogenesis of schizophrenia. However, BDNF levels are not static; in animal experiments, brain BDNF increases during spatial learning, and in clinical depression, successful antidepressant treatment raises serum BDNF. We asked: would neuroplasticity-based cognitive training in schizophrenia result in increased serum BDNF? Fifty-six schizophrenia outpatients and 16 matched healthy comparison subjects were assessed on baseline cognitive performance and serum BDNF. Schizophrenia subjects were randomly assigned to either 50 hours (10 weeks) of computerized auditory training or a computer game control condition, followed by reassessment of cognition and serum BDNF. At baseline, schizophrenia participants had significantly lower-than-normal serum BDNF. Schizophrenia subjects who engaged in computerized cognitive training designed to improve auditory processing showed significant cognitive gains and a significant increase in serum BDNF compared with subjects who played computer games. This increase was evident after 2 weeks of training, and after 10 weeks in the active condition, subjects “normalized” their mean serum BDNF levels, whereas the control group showed no change. In the active condition, change in BDNF was significantly associated with improved quality of life. Serum BDNF levels are significantly increased in clinically stable, chronically ill schizophrenia subjects after neuroplasticity-based cognitive training, but not after computer games. Serum BDNF levels may serve as a peripheral biomarker for the effects of intensive cognitive training and may provide a useful tool for the evaluation of cognitive enhancement methods in schizophrenia.