Could antidepressants increase mood and immunity at the same time?

IF 3.2 3区 医学 Q2 PSYCHIATRY
Frontiers in Psychiatry Pub Date : 2025-03-12 eCollection Date: 2025-01-01 DOI:10.3389/fpsyt.2025.1340179
Francis Lavergne, Therese M Jay
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引用次数: 0

Abstract

A review of scientific literature suggests that the use of antidepressants can be broadly extended to address various forms of stress and inflammation as an adjunctive therapy that enhances host resistance. While the effects of antidepressants on mood are well-documented in terms of their emotional, cognitive, and behavioral impacts, these aspects do not fully explain their cellular mechanisms of action. At the cellular level, antidepressants exert trophic effects that promote neurogenesis and synaptic connectivity. Studies demonstrate that antidepressants improve cell survival, enhance stem cell proliferation, and reduce danger perception (mood effects) in depressed patients and animal models of depression. These trophic properties highlight a deeper biological mechanism beyond their mood-related benefits. The acid sphingomyelinase (ASM) theory of mood offers a more compelling explanation of the cellular effects of antidepressants compared to the monoamine hypothesis. Antidepressants functionally inhibit the ASM enzyme, thereby reducing the production of ceramide, which directs cells toward increased survival, cytoprotection, and reproduction, as well as improved mood. This review also highlights research demonstrating that antidepressants enhance host resistance to infections, immunological challenges, stress, and depression. These findings support the potential use of antidepressants to bolster host resilience in scenarios involving infections, vaccinations, cellular aggression, stress, depression, and even aging.

抗抑郁药能同时改善情绪和免疫力吗?
对科学文献的回顾表明,抗抑郁药的使用可以广泛扩展到解决各种形式的压力和炎症,作为增强宿主抵抗力的辅助治疗。虽然抗抑郁药对情绪的影响在情绪、认知和行为方面都有充分的记录,但这些方面并不能完全解释它们的细胞作用机制。在细胞水平上,抗抑郁药发挥营养作用,促进神经发生和突触连接。研究表明,抗抑郁药物可以改善抑郁症患者和抑郁症动物模型的细胞存活率,增强干细胞增殖,降低危险感知(情绪效应)。这些营养特性强调了它们与情绪相关的益处之外的更深层次的生物学机制。与单胺假说相比,酸性鞘磷脂酶(ASM)理论对抗抑郁药的细胞效应提供了更令人信服的解释。抗抑郁药的功能是抑制ASM酶,从而减少神经酰胺的产生,神经酰胺引导细胞增加存活、细胞保护和繁殖,以及改善情绪。这篇综述还强调了研究表明抗抑郁药可以增强宿主对感染、免疫挑战、压力和抑郁的抵抗力。这些发现支持了抗抑郁药在感染、疫苗接种、细胞攻击、压力、抑郁甚至衰老等情况下增强宿主恢复能力的潜在用途。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Frontiers in Psychiatry
Frontiers in Psychiatry Medicine-Psychiatry and Mental Health
CiteScore
6.20
自引率
8.50%
发文量
2813
审稿时长
14 weeks
期刊介绍: Frontiers in Psychiatry publishes rigorously peer-reviewed research across a wide spectrum of translational, basic and clinical research. Field Chief Editor Stefan Borgwardt at the University of Basel is supported by an outstanding Editorial Board of international researchers. This multidisciplinary open-access journal is at the forefront of disseminating and communicating scientific knowledge and impactful discoveries to researchers, academics, clinicians and the public worldwide. The journal''s mission is to use translational approaches to improve therapeutic options for mental illness and consequently to improve patient treatment outcomes.
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