Neurology Service, James J. Peters Department of Veterans Affairs Medical Center, 130 West Kingsbridge Road, Bronx, NY 10468, USA; Department of Neurology, Icahn School of Medicine at Mount Sinai, One Gustave Levy Place, New York, NY 10029, USA; Department of Psychiatry, Icahn School of Medicine at Mount Sinai, One Gustave Levy Place, New York, NY 10029, USA; Mount Sinai Alzheimer's Disease Research Center and the Ronald M. Loeb Center for Alzheimer's Disease, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.
Department of Neurology, Icahn School of Medicine at Mount Sinai, One Gustave Levy Place, New York, NY 10029, USA; Mount Sinai Alzheimer's Disease Research Center and the Ronald M. Loeb Center for Alzheimer's Disease, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA; Department of Pediatrics, Icahn School of Medicine at Mount Sinai, One Gustave Levy Place, New York, NY 10029, USA.
Neurosci Lett. 2019 Aug 10;707:134294. doi: 10.1016/j.neulet.2019.134294. Epub 2019 May 26.
Traumatic brain injury (TBI) is an unfortunately common event in military life. The conflicts in Iraq and Afghanistan have increased public awareness of TBI in the military. Certain injury mechanisms are relatively unique to the military, the most prominent being blast exposure. Blast-related mild TBI (mTBI) has been of particular concern in the most recent veterans although controversy remains concerning separation of the postconcussion syndrome associated with mTBI from post-traumatic stress disorder. TBI is also a risk factor for the development of neurodegenerative diseases including chronic traumatic encephalopathy (CTE) and Alzheimer's disease (AD). AD, TBI, and CTE are all associated with chronic inflammation. Genome wide association studies (GWAS) have identified multiple genetic loci associated with AD that implicate inflammation and - in particular microglia - as key modulators of the AD- and TBI-related degenerative processes. At the molecular level, recent studies have identified TREM2 and TYROBP/DAP12 as components of a key molecular hub linking inflammation and microglia to the pathophysiology of AD and possibly TBI. Evidence concerning the relationship of TBI to chronic mental health problems and dementia is reviewed in the context of its relevance to military veterans.
创伤性脑损伤(TBI)在军人生活中是一种不幸的常见事件。伊拉克和阿富汗的冲突使公众对军人中的 TBI 有了更多的认识。某些损伤机制在军队中相对独特,最突出的是爆炸暴露。与爆炸相关的轻度 TBI(mTBI)在最近的退伍军人中尤其受到关注,尽管仍然存在争议,即与 mTBI 相关的脑震荡后综合征与创伤后应激障碍分开。TBI 也是神经退行性疾病发展的一个风险因素,包括慢性创伤性脑病(CTE)和阿尔茨海默病(AD)。AD、TBI 和 CTE 都与慢性炎症有关。全基因组关联研究(GWAS)已经确定了多个与 AD 相关的遗传位点,这些位点表明炎症,特别是小胶质细胞,是 AD 和 TBI 相关退行性过程的关键调节剂。在分子水平上,最近的研究已经确定了 TREM2 和 TYROBP/DAP12 作为将炎症和小胶质细胞与 AD 的病理生理学联系起来的关键分子枢纽的组成部分,并且可能与 TBI 也有关。本文在与退伍军人相关的背景下,回顾了 TBI 与慢性心理健康问题和痴呆症之间的关系的证据。