Department Psychiatry Odense, Psychiatry in the Region of Southern Denmark, J.B. Winslowsvej 20, 5000 Odense C, Denmark.
Clinical Neurochemistry, Department Psychiatry and Psychotherapy, University Hospital Würzburg, Fürchsleinstr. 15, 97080 Würzburg, Germany.
Eur Psychiatry. 2017 Oct;46:65-71. doi: 10.1016/j.eurpsy.2017.06.009. Epub 2017 Jul 11.
The neurotrophic factors (NTF) hypothesis of depression was postulated nearly a decade ago and is nowadays widely acknowledged. Previous reports suggest that cerebral concentrations of NTF may be reduced in suicide victims who received minimal or no antidepressant pharmacotherapy. Recent evidence suggests that antidepressant treatment may improve or normalise cerebral concentrations of neurotrophic factors. Therefore, we examined the concentration of brain-derived neurotrophic factor (BDNF) and neurotrophin 3 (NT3) in different brain regions (cortex, cingulate gyrus, thalamus, hippocampus, putamen and nucleus caudatus) of 21 individuals - 7 patients of which 4 patients with major depressive disorder (MDD) and overall age 86.8±5 years who received antidepressant pharmacotherapy (selective serotonin re-uptake inhibitors [SSRI]; tricyclic antidepressants [TCA]), 3 patients with MDD without antidepressant treatment and overall age 84.3±5 years versus 14 unaffected subjects at age 70.3±13.8. We detected significant elevation of BDNF (parietal cortex) and NT3 (parietal, temporal and occipital cortex, cingulate gyrus, thalamus, putamen and nucleus caudatus regions) in MDD patients who received antidepressant medication compared to MDD untreated patients and controls. Moreover, we detected a significant decrease of NT3 levels in the parietal cortex of patients suffering from MDD non-treated patients without treatment compared to healthy individuals. Although the limited statistical power due to the small sample size in this proof of concept study corroborates data from previous studies, which show that treatment with antidepressants mediates alterations in neuroplasticity via the action of NTF. However, more research using post-mortem brain tissue with larger samples needs to be carried out as well as longitudinal studies to further verify these results.
抑郁症的神经营养因子（NTF）假说在近十年前被提出，目前已被广泛认可。之前的报告表明，接受最低剂量或未接受抗抑郁药物治疗的自杀者大脑中的 NTF 浓度可能降低。最近的证据表明，抗抑郁治疗可能会改善或使神经营养因子的大脑浓度正常化。因此，我们检查了 21 个人的不同大脑区域（皮质、扣带回、丘脑、海马体、壳核和尾状核）中的脑源性神经营养因子（BDNF）和神经营养因子 3（NT3）的浓度 - 7 名患者，其中 4 名患有重度抑郁症（MDD），年龄为 86.8±5 岁，接受抗抑郁药物治疗（选择性 5-羟色胺再摄取抑制剂 [SSRIs]；三环抗抑郁药 [TCAs]），3 名患有 MDD 且未接受抗抑郁治疗，年龄为 84.3±5 岁，14 名未受影响的患者年龄为 70.3±13.8 岁。我们发现，接受抗抑郁药物治疗的 MDD 患者的 BDNF（顶叶皮质）和 NT3（顶叶、颞叶和枕叶皮质、扣带回、丘脑、壳核和尾状核区域）水平显著升高，与未接受治疗的 MDD 患者和对照组相比。此外，我们发现，与健康个体相比，未接受治疗的 MDD 患者的顶叶皮质中的 NT3 水平显著降低。尽管由于本概念验证研究的样本量较小，统计能力有限，但这项研究的结果与之前的研究结果一致，这些研究表明，抗抑郁治疗通过 NTF 的作用介导神经可塑性的改变。然而，需要使用更大样本量的死后脑组织进行更多研究，以及进行纵向研究，以进一步验证这些结果。
