Depression following a traumatic brain injury: uncovering cytokine dysregulation as a pathogenic mechanism.
Depression following a traumatic brain injury: uncovering cytokine dysregulation as a pathogenic mechanism.
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DOI：
10.4103/1673-5374.238604
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发表时间：
2018-10
影响因子：
6.1
通讯作者：
Bachstetter AD
中科院分区：
文献类型：
--
作者：
Bodnar CN;Morganti JM;Bachstetter AD
大量的个体具有创伤性脑损伤（TBI）的长期不良影响。抑郁症是影响生活许多方面的长期并发症之一。抑郁症会限制重返工作岗位的能力，甚至会恶化认知功能，导致痴呆症。与TBI相关的抑郁风险增加的机械原因仍有待确定。由于TBI导致慢性神经炎症，并引发胶质细胞的二次挑战，抑郁症的炎症理论提供了一个有前途的框架，调查抑郁症的原因TBI后。TBI后，与一般人群中抑郁症中观察到的细胞因子类似的细胞因子增加也会增加。细胞因子的生物标志物水平在损伤后数小时至数天内达到峰值，但促炎细胞因子仍可能在TBI后数月至数年内升高至生理水平以上，这是TBI后抑郁症可能持续的时间范围。由于肿瘤坏死因子α和白细胞介素1可直接在神经元突触处发出信号，这些细胞因子的病理生理水平可间接改变神经元突触生理学。这篇综述的目的是概述目前的证据，特别是抑郁症的炎症假说，因为它涉及到抑郁症后TBI。此外，我们将阐明肿瘤坏死因子α和白细胞介素1可能导致抑郁症的潜在突触机制。炎症与抑郁症的发展之间的关联是令人信服的;然而，在TBI后抑郁症的背景下，炎症的作用尚未得到充分研究。本综述试图强调了解和治疗TBI心理并发症的必要性，可能通过神经免疫调节来治疗，因为神经精神障碍可能对损伤的康复和整体生活质量产生很大影响。
A substantial number of individuals have long-lasting adverse effects from a traumatic brain injury (TBI). Depression is one of these long-term complications that influences many aspects of life. Depression can limit the ability to return to work, and even worsen cognitive function and contribute to dementia. The mechanistic cause for the increased depression risk associated with a TBI remains to be defined. As TBI results in chronic neuroinflammation, and priming of glia to a secondary challenge, the inflammatory theory of depression provides a promising framework for investigating the cause of depression following a TBI. Increases in cytokines similar to those seen in depression in the general population are also increased following a TBI. Biomarker levels of cytokines peak within hours-to-days after the injury, yet pro-inflammatory cytokines may still be elevated above physiological levels months-to-years following TBI, which is the time frame in which post-TBI depression can persist. As tumor necrosis factor α and interleukin 1 can signal directly at the neuronal synapse, pathophysiological levels of these cytokines can detrimentally alter neuronal synaptic physiology. The purpose of this review is to outline the current evidence for the inflammatory hypothesis of depression specifically as it relates to depression following a TBI. Moreover, we will illustrate the potential synaptic mechanisms by which tumor necrosis factor α and interleukin 1 could contribute to depression. The association of inflammation with the development of depression is compelling; however, in the context of post-TBI depression, the role of inflammation is understudied. This review attempts to highlight the need to understand and treat the psychological complications of a TBI, potentially by neuroimmune modulation, as the neuropsychiatric disabilities can have a great impact on the rehabilitation from the injury, and overall quality of life.
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DOI：
10.1523/jneurosci.5399-12.2013
发表时间：
2013-04-03
期刊：
The Journal of neuroscience : the official journal of the Society for Neuroscience
影响因子：
--
作者：
Bachstetter AD;Rowe RK;Kaneko M;Goulding D;Lifshitz J;Van Eldik LJ
通讯作者：
Van Eldik LJ
DOI：
10.1073/pnas.0510802103
发表时间：
2006-02-21
影响因子：
11.1
作者：
Davis, CN;Mann, E;Bartfai, T
通讯作者：
Bartfai, T
影响因子：
5.3
作者：
Burda JE;Bernstein AM;Sofroniew MV
通讯作者：
Sofroniew MV
影响因子：
5.3
作者：
Bertani, Ilaria;Iori, Valentina;Chiesa, Roberto
通讯作者：
Chiesa, Roberto
影响因子：
64.3
作者：
Chekroud, Adam Mourad;Zotti, Ryan Joseph;Corlett, Philip Robert
通讯作者：
Corlett, Philip Robert