Lotrich Francis E
University of Pittsburgh Medical Center, Western Psychiatric Institute and Clinics, 3811 Ohara Street, Pittsburgh, PA 15213, USA.
Brain Res. 2015 Aug 18;1617:113-25. doi: 10.1016/j.brainres.2014.06.032. Epub 2014 Jul 5.
Inflammatory cytokines can sometimes trigger depression in humans, are often associated with depression, and can elicit some behaviors in animals that are homologous to major depression. Moreover, these cytokines can affect monoaminergic and glutamatergic systems, supporting an overlapping pathoetiology with major depression. This suggests that there could be a specific major depression subtype, inflammatory cytokine-associated depression (ICAD), which may require different therapeutic approaches. However, most people do not develop depression, even when exposed to sustained elevations in inflammatory cytokines. Thus several vulnerabilities and sources of resilience to inflammation-associated depression have been identified. These range from genetic differences in neurotrophic and serotonergic systems to sleep quality and omega-3 fatty acid levels. Replicating these sources of resilience as treatments could be one approach for preventing "ICAD". This article is part of a Special Issue entitled SI: Neuroimmunology in Health And Disease.
炎症细胞因子有时会引发人类的抑郁症，常与抑郁症相关联，并且能在动物身上引发一些与重度抑郁症相似的行为。此外，这些细胞因子会影响单胺能和谷氨酸能系统，支持了与重度抑郁症重叠的病理病因学。这表明可能存在一种特定的重度抑郁症亚型，即炎症细胞因子相关抑郁症（ICAD），它可能需要不同的治疗方法。然而，即使暴露于炎症细胞因子持续升高的环境中，大多数人也不会患上抑郁症。因此，已经确定了几种对炎症相关抑郁症的易感性和恢复力来源。这些范围从神经营养和血清素能系统的基因差异到睡眠质量和ω-3脂肪酸水平。将这些恢复力来源复制作为治疗方法可能是预防“ICAD”的一种途径。本文是名为《健康与疾病中的神经免疫学》特刊的一部分。
