Inflammaging, cellular senescence, and cognitive aging after traumatic brain injury.
Inflammaging, cellular senescence, and cognitive aging after traumatic brain injury.
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DOI：
10.1016/j.nbd.2023.106090
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发表时间：
2023-05
影响因子：
6.1
通讯作者：
Dhandapani, Krishnan M.
中科院分区：
文献类型：
--
作者：
Lu, Yujiao;Jarrahi, Abbas;Moore, Nicholas;Bartoli, Manuela;Brann, Darrell W.;Baban, Babak;Dhandapani, Krishnan M.
创伤性脑损伤在世界范围内与死亡率和发病率有关。积累的临床前和临床数据表明，脑外伤是进行性神经变性的主要外因。无论是单次中重度或反复轻度脑损伤后的神经恶化，在老年人群中通常类似于痴呆症；然而，目前还没有批准的治疗方法足以缓解神经退行性变。炎症与脑损伤后多年的神经退行性改变和认知功能障碍相关，提示免疫激活与年龄和脑损伤导致的认知功能下降之间存在潜在的关联。炎症是一种与自然衰老相关的慢性、低级别无菌炎症，会促进认知能力下降。细胞衰老和随后的衰老相关分泌表型(SASP)的发展促进了炎症和认知老化，尽管脑损伤后衰老细胞和神经变性之间的功能联系尚不清楚。在这篇简短的综述中，我们提供了临床前和临床证据的概述，这些证据将细胞衰老与糟糕的脑外伤预后联系在一起。我们还讨论了目前的知识和未来的潜在治疗方法，包括感觉剂和感觉剂，它可以杀死和/或调节衰老细胞，作为脑外伤后的潜在治疗方法。
Traumatic brain injury (TBI) is associated with mortality and morbidity worldwide. Accumulating pre-clinical and clinical data suggests TBI is the leading extrinsic cause of progressive neurodegeneration. Neurological deterioration after either a single moderate-severe TBI or repetitive mild TBI often resembles dementia in aged populations; however, no currently approved therapies adequately mitigate neurodegeneration. Inflammation correlates with neurodegenerative changes and cognitive dysfunction for years post-TBI, suggesting a potential association between immune activation and both age- and TBI-induced cognitive decline. Inflammaging, a chronic, low-grade sterile inflammation associated with natural aging, promotes cognitive decline. Cellular senescence and the subsequent development of a senescence associated secretory phenotype (SASP) promotes inflammaging and cognitive aging, although the functional association between senescent cells and neurodegeneration is poorly defined after TBI. In this mini-review, we provide an overview of the pre-clinical and clinical evidence linking cellular senescence with poor TBI outcomes. We also discuss the current knowledge and future potential for senotherapeutics, including senolytics and senomorphics, which kill and/or modulate senescent cells, as potential therapeutics after TBI.
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影响因子：
13.8
作者：
通讯作者：
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影响因子：
5.3
作者：
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通讯作者：
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影响因子：
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DOI：
10.1016/j.bbrc.2019.03.199
发表时间：
2019-05-28
影响因子：
3.1
作者：
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通讯作者：
Chini, Eduardo