Major depressive disorder (MDD) is a leading cause of morbidity, and the fourth leading cause of disease burden worldwide. While MDD is a treatable condition for many individuals, others suffer from treatment-resistant depression (TRD). Here, we suggest the immunomodulatory compound AS101 as novel therapeutic alternative. We previously showed in animal models that AS101 reduces anxiety-like behavior and elevates levels of the brain-derived neurotrophic factor (BDNF), a protein that has a key role in the pathophysiology of depression. To explore the potential antidepressant properties of AS101, we used the extensively characterized chronic mild stress (CMS) model, and the depressive rat line (DRL Finally, in Exp. 3 to attain insight into the mechanism we knocked down BDNF in the hippocampus, and demonstrated that the beneficial effect of AS101 was abrogated. Together with the previously established safety profile of AS101 in humans, these results may represent the first step towards the development of a novel treatment option for MDD and TRD.

中文翻译：

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基于碲的小免疫调节分子可改善两种不同大鼠模型的抑郁样行为。

重度抑郁症 (MDD) 是发病的主要原因，也是全球疾病负担的第四大原因。虽然 MDD 对许多人来说是一种可治疗的疾病，但其他人患有难治性抑郁症 (TRD)。在这里，我们建议将免疫调节化合物 AS101 作为新的治疗选择。我们之前在动物模型中表明，AS101 可减少焦虑样行为并提高脑源性神经营养因子 (BDNF) 的水平，BDNF 是一种在抑郁症的病理生理学中起关键作用的蛋白质。为了探索 AS101 的潜在抗抑郁特性，我们使用了广泛表征的慢性轻度应激 (CMS) 模型和抑郁大鼠系（DRL 最后，在实验 3 中，以深入了解我们在海马中敲除 BDNF 的机制，并证明 AS101 的有益作用被废除。连同先前建立的 AS101 在人类中的安全性特征，这些结果可能代表着开发 MDD 和 TRD 的新型治疗方案的第一步。