Inflammatory cytokine-associated depression.

Inflammatory cytokine-associated depression.
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DOI:
10.1016/j.brainres.2014.06.032
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发表时间:
2015-08-18
期刊:
影响因子:
2.9
通讯作者:
Lotrich, Francis E.
Lotrich, Francis E.
中科院分区:
医学3区
文献类型:
--
作者:
Lotrich, Francis E.

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炎性细胞因子有时会引发人类抑郁症,通常与抑郁症有关,并且可以在动物中引发一些与重度抑郁症同源的行为。此外,这些细胞因子可以影响单胺能和多巴胺能系统,支持与重性抑郁症重叠的病因。这表明可能存在一种特定的重度抑郁症亚型,即炎性神经递质相关抑郁症(ICAD),可能需要不同的治疗方法。然而,大多数人不会患上抑郁症,即使是在炎症细胞因子持续升高的情况下。因此,已经确定了炎症相关抑郁症的几个脆弱性和恢复力来源。这些差异包括神经营养和多巴胺能系统的遗传差异,睡眠质量和ω-3脂肪酸水平。复制这些恢复力的来源作为治疗方法可能是预防“ICAD”的一种方法。
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”.
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