The Impact of Aerobic Exercise on Brain-Derived Neurotrophic Factor and Neurocognition in Individuals With Schizophrenia: A Single-Blind, Randomized Clinical Trial

The Impact of Aerobic Exercise on Brain-Derived Neurotrophic Factor and Neurocognition in Individuals With Schizophrenia: A Single-Blind, Randomized Clinical Trial
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DOI:
10.1093/schbul/sbv022
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发表时间:
2015-07-01
影响因子:
6.6
通讯作者:
Sloan, Richard P.
Sloan, Richard P.
中科院分区:
医学1区
文献类型:
--
作者:
Kimhy, David;Vakhrusheva, Julia;Sloan, Richard P.

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精神分裂症患者表现出严重的神经认知缺陷,现有的治疗方法只能提供有限的益处。然而,对动物、临床和非临床人群的研究发现,通过有氧运动训练(AE),神经认知的改善与有氧健身(AF)的增加有关。这种改善归因于脑源性神经营养因子(BDNF)的上调。然而,AE对神经认知的影响以及BDNF的作用尚未在精神分裂症中得到研究。采用概念验证、单盲、随机临床试验设计,33名精神分裂症患者随机接受标准精神治疗(n = 17;“常规治疗”;TAU)或参加为期12周的AE项目(n = 16),使用主动游戏视频游戏(Xbox 360 Kinect)和传统AE设备。参与者在12周前后完成了AF(以VO2峰值ml/kg/min为指标)、神经认知(matrix共识认知电池)和血清bdnf的评估。26名参与者(79%)完成了研究。在随访中,AE参与者的AF改善了18.0%,而TAU组下降了-0.5% (P = 0.002),神经认知改善了15.1%,而TAU组下降了-2.0% (P = 0.031)。分层多元回归分析显示,AF的增强和BDNF的增加分别预测了25.4%和14.6%的神经认知改善方差。结果表明AE可有效增强精神分裂症患者的神经认知功能,并为AE相关BDNF上调对精神分裂症患者神经认知的影响提供初步支持。不良房颤是精神分裂症患者神经认知功能障碍的一个可改变的危险因素,而房颤训练为其提供了一种安全、无耻辱感和无副作用的干预措施。
Individuals with schizophrenia display substantial neurocognitive deficits for which available treatments offer only limited benefits. Yet, findings from studies of animals, clinical and nonclinical populations have linked neurocognitive improvements to increases in aerobic fitness (AF) via aerobic exercise training (AE). Such improvements have been attributed to up-regulation of brain-derived neurotrophic factor (BDNF). However, the impact of AE on neurocognition, and the putative role of BDNF, have not been investigated in schizophrenia. Employing a proof-of-concept, single-blind, randomized clinical trial design, 33 individuals with schizophrenia were randomized to receive standard psychiatric treatment (n = 17; "treatment as usual"; TAU) or attend a 12-week AE program (n = 16) utilizing active-play video games (Xbox 360 Kinect) and traditional AE equipment. Participants completed assessments of AF (indexed by VO2 peak ml/kg/min), neurocognition (MATRICS Consensus Cognitive Battery), and serum-BDNF before and after and 12-week period. Twenty-six participants (79%) completed the study. At follow-up, the AE participants improved their AF by 18.0% vs a -0.5% decline in the TAU group (P = .002) and improved their neurocognition by 15.1% vs -2.0% decline in the TAU group (P = .031). Hierarchical multiple regression analyses indicated that enhancement in AF and increases in BDNF predicted 25.4% and 14.6% of the neurocognitive improvement variance, respectively. The results indicate AE is effective in enhancing neurocognitive functioning in people with schizophrenia and provide preliminary support for the impact of AE-related BDNF up-regulation on neurocognition in this population. Poor AF represents a modifiable risk factor for neurocognitive dysfunction in schizophrenia for which AE training offer a safe, nonstigmatizing, and side-effect-free intervention.