Contagion of depression: a double-edged sword.

IF 5.8 1区 医学 Q1 PSYCHIATRY Translational Psychiatry Pub Date : 2024-09-30 DOI:10.1038/s41398-024-03124-2
Chen-Wei Huang, Ting Hu, Hong Zheng, Yi-Lin Wu, Jia-Mei Li, Yi-Ming Wang, Wen-Jun Su, Wei Wang, Yun-Zi Liu, Chun-Lei Jiang
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Abstract

Depression is a significant mental health issue with extensive economic implications, and recent studies suggest it may be transmitted between individuals. However, the mechanisms of this contagion remain unclear, and the social buffering effect has been understudied. This research employs three rodent models, including stress crossover, cohabitation-induced, and non-contact induced depression contagion models, to explore these mechanisms. Here, we report that that naive mice cohabiting with depressed mice showed increased corticosterone levels and depressive behaviors, unlike those with stressed mice, who did not exhibit these changes and even mitigated desperation in stressed mice. Non-contact cohabitation did not produce significant behavioral differences, but exposure to bedding from depressed mice reduced sucrose preference in naive mice. This study introduces reliable models of depression contagion, suggesting it operates independently of stress transmission. The interplay between depression contagion and social buffering may vary in different contexts. These findings provide new insights into the mechanisms of depression contagion and potential strategies for preventing depressive disorders.

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抑郁症的传染:一把双刃剑。
抑郁症是一个严重的心理健康问题,对经济有着广泛的影响,最近的研究表明,抑郁症可能会在人与人之间传播。然而,这种传染的机制仍不清楚,社会缓冲效应也未得到充分研究。本研究采用了三种啮齿动物模型,包括压力交叉模型、同居诱导模型和非接触诱导抑郁传染模型,来探索这些机制。在这里,我们报告说,与抑郁小鼠同居的天真小鼠表现出皮质酮水平升高和抑郁行为,而与应激小鼠同居的天真小鼠则不同,它们没有表现出这些变化,甚至减轻了应激小鼠的绝望情绪。非接触式同居不会产生显著的行为差异,但接触抑郁小鼠的垫料会降低天真小鼠的蔗糖偏好。这项研究引入了抑郁传染的可靠模型,表明抑郁传染的运作与应激传递无关。抑郁传染和社会缓冲之间的相互作用可能在不同的环境中有所不同。这些发现为抑郁传染机制和预防抑郁障碍的潜在策略提供了新的见解。
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来源期刊
CiteScore
11.50
自引率
2.90%
发文量
484
审稿时长
23 weeks
期刊介绍: Psychiatry has suffered tremendously by the limited translational pipeline. Nobel laureate Julius Axelrod''s discovery in 1961 of monoamine reuptake by pre-synaptic neurons still forms the basis of contemporary antidepressant treatment. There is a grievous gap between the explosion of knowledge in neuroscience and conceptually novel treatments for our patients. Translational Psychiatry bridges this gap by fostering and highlighting the pathway from discovery to clinical applications, healthcare and global health. We view translation broadly as the full spectrum of work that marks the pathway from discovery to global health, inclusive. The steps of translation that are within the scope of Translational Psychiatry include (i) fundamental discovery, (ii) bench to bedside, (iii) bedside to clinical applications (clinical trials), (iv) translation to policy and health care guidelines, (v) assessment of health policy and usage, and (vi) global health. All areas of medical research, including — but not restricted to — molecular biology, genetics, pharmacology, imaging and epidemiology are welcome as they contribute to enhance the field of translational psychiatry.
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