Progressive inflammation-mediated neurodegeneration after traumatic brain or spinal cord injury

被引:225
|
作者
Faden, Alan I. [1 ]
Wu, Junfang [1 ]
Stoica, Bogdan A. [1 ]
Loane, David J. [1 ]
机构
[1] Univ Maryland, Sch Med, Ctr Shock Trauma & Anesthesiol Res STAR, Dept Anesthesiol, S247,20 Penn St, Baltimore, MD 21201 USA
关键词
MICROGLIA/MACROPHAGE POLARIZATION DYNAMICS; AMYLOID PROTEIN DEPOSITION; CENTRAL NEUROPATHIC PAIN; DEFAULT MODE NETWORK; MICROGLIAL ACTIVATION; CORTICOSPINAL NEURONS; ALZHEIMERS-DISEASE; DIFFUSION-TENSOR; CONCISE GUIDE; WHITE-MATTER;
D O I
10.1111/bph.13179
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Traumatic brain injury (TBI) has been linked to dementia and chronic neurodegeneration. Described initially in boxers and currently recognized across high contact sports, the association between repeated concussion (mild TBI) and progressive neuropsychiatric abnormalities has recently received widespread attention, and has been termed chronic traumatic encephalopathy. Less well appreciated are cognitive changes associated with neurodegeneration in the brain after isolated spinal cord injury. Also under-recognized is the role of sustained neuroinflammation after brain or spinal cord trauma, even though this relationship has been known since the 1950s and is supported by more recent preclinical and clinical studies. These pathological mechanisms, manifested by extensive microglial and astroglial activation and appropriately termed chronic traumatic brain inflammation or chronic traumatic inflammatory encephalopathy, may be among the most important causes of post-traumatic neurodegeneration in terms of prevalence. Importantly, emerging experimental work demonstrates that persistent neuroinflammation can cause progressive neurodegeneration that may be treatable even weeks after traumatic injury. Linked ArticlesThis article is part of a themed section on Inflammation: maladies, models, mechanisms and molecules. To view the other articles in this section visit
引用
收藏
页码:681 / 691
页数:11
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