A Levee to the Flood: Pre-injury Neuroinflammation and Immune Stress Influence Traumatic Brain Injury Outcome.
A Levee to the Flood: Pre-injury Neuroinflammation and Immune Stress Influence Traumatic Brain Injury Outcome.
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DOI：
10.3389/fnagi.2021.788055
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发表时间：
2021
影响因子：
4.8
通讯作者：
Kokiko-Cochran ON
中科院分区：
文献类型：
--
作者：
Houle S;Kokiko-Cochran ON
越来越多的证据表明，衰老影响大脑对创伤性脑损伤(TBI)的反应，为阿尔茨海默病(AD)等神经退行性病理奠定了基础。这个话题经常被关于损伤后衰老和炎症的讨论所主导，这可能会减少对创伤性脑损伤前这些相同因素的考虑。事实上，脑外伤前的衰老和炎症可能在调节预后方面也同样重要。例如，在所有严重程度中，老年人的脑损伤发生率最高。此外，损伤前的免疫挑战或应激源可能会改变病理和预后，而不受年龄的影响。对脑外伤的炎症反应是可塑性的，并受到先前、一致和随后的免疫侮辱的影响。因此，引发或包括炎症反应的预先存在的疾病可能会极大地影响大脑对创伤的反应能力，并最终影响慢性结局。本综述的目的是详细介绍与年龄相关的细胞和分子变化，以及AD的遗传风险变异如何影响脑外伤后的神经炎性反应。首先，我们将回顾颅脑损伤后神经炎症的来源和病理。然后，我们将强调与年龄相关的内源性炎症来源的重要性，包括细胞因子表达、活性氧处理和线粒体功能的变化。人们高度关注线粒体，认为它是炎症和阿尔茨海默病各种遗传风险因素之间不可或缺的联系。综上所述，这篇综述将汇编当前的临床和实验研究，以强调与感染和应激、衰老和遗传风险因素相关的先前存在的炎症变化如何改变对脑外伤的反应。
Increasing evidence demonstrates that aging influences the brain's response to traumatic brain injury (TBI), setting the stage for neurodegenerative pathology like Alzheimer's disease (AD). This topic is often dominated by discussions of post-injury aging and inflammation, which can diminish the consideration of those same factors before TBI. In fact, pre-TBI aging and inflammation may be just as critical in mediating outcomes. For example, elderly individuals suffer from the highest rates of TBI of all severities. Additionally, pre-injury immune challenges or stressors may alter pathology and outcome independent of age. The inflammatory response to TBI is malleable and influenced by previous, coincident, and subsequent immune insults. Therefore, pre-existing conditions that elicit or include an inflammatory response could substantially influence the brain's ability to respond to traumatic injury and ultimately affect chronic outcome. The purpose of this review is to detail how age-related cellular and molecular changes, as well as genetic risk variants for AD affect the neuroinflammatory response to TBI. First, we will review the sources and pathology of neuroinflammation following TBI. Then, we will highlight the significance of age-related, endogenous sources of inflammation, including changes in cytokine expression, reactive oxygen species processing, and mitochondrial function. Heightened focus is placed on the mitochondria as an integral link between inflammation and various genetic risk factors for AD. Together, this review will compile current clinical and experimental research to highlight how pre-existing inflammatory changes associated with infection and stress, aging, and genetic risk factors can alter response to TBI.
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DOI：
10.1016/j.jalz.2018.05.004
发表时间：
2018-09
期刊：
Alzheimer's & dementia : the journal of the Alzheimer's Association
影响因子：
--
作者：
Alosco ML;Tripodis Y;Fritts NG;Heslegrave A;Baugh CM;Conneely S;Mariani M;Martin BM;Frank S;Mez J;Stein TD;Cantu RC;McKee AC;Shaw LM;Trojanowski JQ;Blennow K;Zetterberg H;Stern RA
通讯作者：
Stern RA
影响因子：
--
作者：
Ayala A;Muñoz MF;Argüelles S
通讯作者：
Argüelles S
影响因子：
9.3
作者：
Abdullah A;Zhang M;Frugier T;Bedoui S;Taylor JM;Crack PJ
通讯作者：
Crack PJ
影响因子：
6.3
作者：
Bermpohl, Daniela;You, Zerong;Whalen, Michael J.
通讯作者：
Whalen, Michael J.
影响因子：
11
作者：
Brouwers, N.;Van Cauwenberghe, C.;Engelborghs, S.;Lambert, J-C;Bettens, K.;Le Bastard, N.;Pasquier, F.;Montoya, A. Gil;Peeters, K.;Mattheijssens, M.;Vandenberghe, R.;De Deyn, P. P.;Cruts, M.;Amouyel, P.;Sleegers, K.;Van Broeckhoven, C.
通讯作者：
Van Broeckhoven, C.