BDNF 血液水平是双相抑郁症治疗反应和缓解的潜在生物标志物

Anton Shkundin , James Sinacore , Angelos Halaris
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引用次数: 0

摘要

背景免疫功能障碍和炎症在双相情感障碍的病理生理学中起着至关重要的作用。耐药双相抑郁障碍(TRBDD)给精神科治疗带来了巨大挑战,患者往往对标准治疗策略毫无反应。塞来昔布是一种选择性环氧化酶-2(COX-2)抑制剂,已显示出作为双相抑郁症附加治疗的前景,有可能影响脑源性神经营养因子(BDNF)的水平。方法我们评估了43名被诊断为双相情感障碍I或II的治疗耐受性双相抑郁障碍(TRBDD)患者的治疗对BDNF水平的影响,并将他们的基线BDNF水平与13名健康对照组(HC)的BDNF水平进行了比较。TRBDD患者被随机分配接受为期8周的艾司西酞普兰加安慰剂(ESC + PBO)或艾司西酞普兰加塞来昔布(ESC + CBX)治疗。在基线、第4周和第8周测量血清中的BDNF水平。HC组仅在基线时提供样本。结果TRBDD组的基线平均BDNF水平明显低于HC组(p = 0.015),这表明BDNF在TRBDD的病理生理学中可能发挥作用。然而,在TRBDD组中,无论接受ESC + PBO还是ESC + CBX治疗,基线、第4周和第8周的BDNF水平在应答者和非应答者之间、缓解者和非缓解者之间均无显著差异。我们的研究表明,在研究期间,艾司西酞普兰和塞来昔布并未对BDNF水平产生显著变化。有必要进行样本量更大、随访时间更长的进一步研究,以探讨这些治疗方法对TRBDD患者BDNF水平的影响,并评估将BDNF水平作为治疗反应和缓解的生物标志物的使用情况。
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BDNF blood levels as a potential biomarker Predictor of treatment response and remission in bipolar depression

Background

Immune dysfunction and inflammation play critical roles in the pathophysiology of bipolar disorder. Treatment-resistant bipolar depressive disorder (TRBDD) poses significant challenges in psychiatric practice, often unresponsive to standard treatment strategies. Celecoxib, a selective Cyclooxygenase-2 (COX-2) inhibitor, has shown promise as an add-on treatment for bipolar depression, potentially influencing brain-derived neurotrophic factor (BDNF) levels.

Methods

We assessed the effects of treatment on BDNF levels in 43 patients with Treatment-Resistant Bipolar Depressive Disorder (TRBDD), diagnosed with Bipolar Disorder I or II, and compared their baseline BDNF levels with those of 13 healthy control (HC) individuals. TRBDD participants were randomized to receive either Escitalopram plus Placebo (ESC + PBO) or Escitalopram with Celecoxib (ESC + CBX) for 8 weeks. BDNF levels in serum were measured at baseline, week 4, and week 8. The HC group only provided samples at baseline. Statistical analyses were conducted to compare BDNF levels between TRBDD and HC groups, as well as between TRBDD participants in the ESC + PBO and ESC + CBX groups, in relation to treatment response and remission.

Results

The TRBDD group demonstrated significantly lower baseline mean BDNF levels compared to the HC group (p = 0.015), suggesting a potential role for BDNF in the pathophysiology of TRBDD. However, BDNF levels at baseline, week 4, and week 8 did not differ significantly between responders and non-responders, or between remitters and non-remitters, within the TRBDD group, regardless of whether they were receiving ESC + PBO or ESC + CBX treatment.

Conclusions

The significant difference in baseline BDNF levels between TRBDD patients and healthy controls highlights the potential importance of BDNF in the pathophysiology of TRBDD. Our study suggests that Escitalopram with Celecoxib did not produce significant changes in BDNF levels over the study period. Further research with larger sample sizes and extended follow-up periods is necessary to explore the effects of these treatments on BDNF levels in TRBDD patients and to evaluate the use of BDNF levels as biomarkers for treatment response and remission.
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