The immunology of traumatic brain injury: a prime target for Alzheimer's disease prevention.
The immunology of traumatic brain injury: a prime target for Alzheimer's disease prevention.
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DOI：
10.1186/1742-2094-9-185
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发表时间：
2012-08-01
影响因子：
9.3
通讯作者：
Tan J
中科院分区：
文献类型：
--
作者：
Giunta B;Obregon D;Velisetty R;Sanberg PR;Borlongan CV;Tan J
创伤性脑损伤（TBI）是一个全球性的健康问题，在当今世界军事冲突不断的时代尤为普遍。其病理学标志是一个或多个原发性损伤灶，随后通过炎性细胞因子和趋化因子的级联扩散到最初正常的脑区域，导致小胶质细胞和其他中枢神经系统免疫细胞对原始组织损伤的放大。在某些情况下，这可能使个体更容易发展为阿尔茨海默病（AD）。TBI的炎症性进展已被证明在TBI后长达17年的人类中是活跃的。不幸的是，所有的神经保护药物试验都失败了，具体的治疗方法仍然不够有效。这些糟糕的结果可能是由于科学上过于关注神经元而没有解决大脑中小胶质细胞的功能，而小胶质细胞是促炎细胞因子产生的中心。为了解决这个问题，我们提供了一个调查TBI相关的脑免疫机制，可能会促进进展到AD。我们讨论了这些免疫和小胶质细胞为基础的炎症机制参与创伤后脑损伤的进展，以AD。类黄酮为基础的策略，以反对抗原呈递细胞样炎性表型的小胶质细胞也将进行审查。目的是为TBI后炎症反应的研究提供理论依据，TBI可能代表与AD的病理联系。最后，更好地了解神经炎症可以为消除继发性细胞死亡和行为症状开辟治疗途径，这些症状可能介导TBI向后期AD的进展。
A global health problem, traumatic brain injury (TBI) is especially prevalent in the current era of ongoing world military conflicts. Its pathological hallmark is one or more primary injury foci, followed by a spread to initially normal brain areas via cascades of inflammatory cytokines and chemokines resulting in an amplification of the original tissue injury by microglia and other central nervous system immune cells. In some cases this may predispose individuals to later development of Alzheimer’s disease (AD). The inflammatory-based progression of TBI has been shown to be active in humans for up to 17 years post TBI. Unfortunately, all neuroprotective drug trials have failed, and specific treatments remain less than efficacious. These poor results might be explained by too much of a scientific focus on neurons without addressing the functions of microglia in the brain, which are at the center of proinflammatory cytokine generation. To address this issue, we provide a survey of the TBI-related brain immunological mechanisms that may promote progression to AD. We discuss these immune and microglia-based inflammatory mechanisms involved in the progression of post-trauma brain damage to AD. Flavonoid-based strategies to oppose the antigen-presenting cell-like inflammatory phenotype of microglia will also be reviewed. The goal is to provide a rationale for investigations of inflammatory response following TBI which may represent a pathological link to AD. In the end, a better understanding of neuroinflammation could open therapeutic avenues for abrogation of secondary cell death and behavioral symptoms that may mediate the progression of TBI to later AD.
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影响因子：
9.3
作者：
Dirscherl K;Karlstetter M;Ebert S;Kraus D;Hlawatsch J;Walczak Y;Moehle C;Fuchshofer R;Langmann T
通讯作者：
Langmann T
影响因子：
14
作者：
Brookmeyer, Ron;Johnson, Elizabeth;Arrighi, H. Michael
通讯作者：
Arrighi, H. Michael
影响因子：
5.7
作者：
FERINISTRAMBI, L;SMIRNE, S;FRANCESCHI, M
通讯作者：
FRANCESCHI, M
影响因子：
9.9
作者：
AMADUCCI, LA;FRATIGLIONI, L;SCHOENBERG, BS
通讯作者：
SCHOENBERG, BS
影响因子：
--
作者：
DeKosky, Steven T.;Abrahamson, Eric E.;Ikonomovic, Milos D.
通讯作者：
Ikonomovic, Milos D.