Inflammatory Depression-Mechanisms and Non-Pharmacological Interventions.

Inflammatory Depression-Mechanisms and Non-Pharmacological Interventions.
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炎症性抑郁--机制和非药理学干预。

DOI:
10.3390/ijms22041640
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发表时间:
2021-02-06
影响因子:
5.6
通讯作者:
Lindqvist D
Lindqvist D
中科院分区:
生物学2区
文献类型:
--
作者:
Suneson K;Lindahl J;Chamli Hårsmar S;Söderberg G;Lindqvist D

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抑郁症的治疗受到未能识别具有不同病理生理学的不同症状特征的阻碍,这些症状特征对不同的治疗有不同的反应。我们认为炎症性抑郁症是一种有意义的抑郁症亚型,与特定的症状和生物学异常相关。我们回顾了几个上游,潜在的致病机制,驱动低度炎症在这种亚型的抑郁症。我们还讨论了调节炎症和抑郁症症状之间联系的下游机制,包括多巴胺能神经传递和色氨酸代谢的改变。最后,我们回顾了几种非药物干预炎症性抑郁症的证据,包括益生菌,ω-3脂肪酸和体育锻炼干预。虽然一些证据表明,这些干预措施可能对炎症性抑郁症有效,但未来的临床试验应考虑丰富患者人群的炎症标志物,或根据炎症状态对患者进行分层,以证实或反驳这一假设。
Treatment of depression is hampered by the failure to identify distinct symptom profiles with distinct pathophysiologies that differentially respond to distinct treatments. We posit that inflammatory depression is a meaningful depression subtype associated with specific symptoms and biological abnormalities. We review several upstream, potentially causative, mechanisms driving low-grade inflammation in this subtype of depression. We also discuss downstream mechanisms mediating the link between inflammation and symptoms of depression, including alterations in dopaminergic neurotransmission and tryptophan metabolism. Finally, we review evidence for several non-pharmacological interventions for inflammatory depression, including probiotics, omega-3 fatty acids, and physical exercise interventions. While some evidence suggests that these interventions may be efficacious in inflammatory depression, future clinical trials should consider enriching patient populations for inflammatory markers, or stratify patients by inflammatory status, to confirm or refute this hypothesis.
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