Serum brain-derived neurotrophic factor levels in relation to comorbid depression and cytokine levels in Nepalese men with alcohol-use disorders.
Serum brain-derived neurotrophic factor levels in relation to comorbid depression and cytokine levels in Nepalese men with alcohol-use disorders.
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DOI：
10.1016/j.alcohol.2015.01.012
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发表时间：
2015-08
期刊：
影响因子：
2.3
通讯作者：
S. Neupane;L. Lien;T. Ueland;T. Mollnes;P. Aukrust;J. Bramness
中科院分区：
文献类型：
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作者：
S. Neupane;L. Lien;T. Ueland;T. Mollnes;P. Aukrust;J. Bramness
神经退行性和炎症过程分别涉及重性抑郁症（MD）和酒精使用障碍（AUD）。在共病AUD和抑郁症的背景下，这种关系的性质知之甚少。在这项研究中，我们测定了AUD患者血清脑源性神经营养因子（BDNF）水平，并测试了BDNF水平是否与抑郁症病史、近期抑郁症状、AUD严重程度以及TNF-α和IL-6水平相关。对平均戒酒34天的尼泊尔男性AUD住院患者（N= 152）进行结构化访谈，以评估抑郁症状、饮酒模式和程度，并对AUD和MD进行研究诊断。通过酒精使用障碍识别测试的评分评估AUD严重程度。血清BDNF和细胞因子分别用ELISA和多重技术检测。虽然血清BDNF水平与MD病史无关，但近期有抑郁症状的患者（n= 42）（平均值± SD）BDNF血清水平与无BDNF血清水平相比（n= 110）（21.6 ± 8.1 ng/mL vs. 26.0 ± 9.6 ng/mL; p= 0.010），与AUD严重程度较低且无酗酒的患者相比，AUD严重程度较高且有酗酒模式的患者的平均血清BDNF水平较高。（分别为25.9 ± 9.7 ng/mL和22.1 ± 8.7 ng/mL;p= 0.022和25.7 ± 9.3和21.8 ± 9.7 ng/mL;p= 0.029）。BDNF与TNF-α（r= 0.39，p < 0.001）和IL-6（r= 0.2，p = 0.027）呈正相关。特别是，在控制混杂因素后，TNF-α水平可预测BDNF水平（B= 0.3 [95% CI = 0.2-0.5]，p< 0.001）。这些发现表明，在饮酒人群中，外周BDNF水平与AUD的严重程度以及抑郁症状的存在有关。炎症因子和神经营养因子之间的显著相关性可能对AUD恢复期间的神经适应性变化有影响。
Neurodegenerative and inflammatory processes are involved separately in major depression (MD) and alcohol-use disorders (AUD). Little is known about the nature of this relationship in the context of comorbid AUD and depression disorders. In this study, we determined brain-derived neurotrophic factor (BDNF) serum levels in patients with AUD and tested whether BDNF levels were related to history of major depression, recent depressive symptoms, AUD severity, and TNF-α and IL-6 levels. Nepalese male AUD inpatients (N= 152) abstinent from alcohol for an average of 34 days were administered structured interviews to assess depression symptoms and pattern and extent of alcohol use, and to generate research diagnoses for AUD and MD. AUD severity was assessed by scores on the Alcohol Use Disorder Identification Test. Serum BDNF and cytokines were measured using ELISA and multiplex technology, respectively. Although serum BDNF levels were unrelated to MD history, patients with recent depressive symptoms (n= 42) had lower (mean ± SD) BDNF serum levels compared to those without (n= 110) (21.6 ± 8.1 ng/mL vs. 26.0 ± 9.6 ng/mL;p= 0.010), and patients with higher AUD severity and binge-drinking patterns had higher mean serum BDNF levels compared to lower AUD severity and non-binging (25.9 ± 9.7 ng/mL vs. 22.1 ± 8.7 ng/mL;p= 0.022 and 25.7 ± 9.3 vs. 21.8 ± 9.7 ng/mL;p= 0.029, respectively). Positive correlations were present between BDNF and TNF-α (r= 0.39,p< 0.001) and IL-6 (r= 0.2,p= 0.027). In particular, TNF-α levels were predictive of BDNF levels after controlling for confounders (B= 0.3 [95% CI = 0.2–0.5],p< 0.001). These findings show that in alcohol-using populations, peripheral BDNF levels are related to severity of AUD as well as presence of depressive symptoms. The significant associations between inflammatory and neurotrophic factors may have implications for neuroadaptive changes during recovery from AUD.