[1] Maas A I R, Stocchetti N, Bullock R. Moderate and severe traumatic brain injury in adults[J]. Lancet Neurol, 2008, 7(8):728-741. [2] Rabinowitz A R, Levin H S. Cognitive sequelae of traumatic brain injury[J]. Psychiatr Clin North Am, 2014, 37(1):1-11. [3] Sivanandam T M, Thakur M K. Traumatic brain injury:a risk factor for Alzheimer's disease[J]. Neurosci Biobehav Rev, 2012, 36(5):1376-1381. [4] Ikonomovic M D, Uryu K, Abrahamson E E, et al. Alzheimer's pathology in human temporal cortex surgically excised after severe brain injury[J]. Exp Neurol, 2004, 190(1):192-203. [5] Uryu K, Chen X H, Martinez D, et al. Multiple proteins implicated in neurodegenerative diseases accumulate in axons after brain trauma in humans[J]. Exp Neurol, 2007, 208(2):185-192. [6] Hawkins B E, Krishnamurthy S, Castillo-Carranza D L, et al. Rapid accumulation of endogenous tau oligomers in a rat model of traumatic brain injury[J]. J Biol Chem, 2013, 288(23):17042-17050. [7] 王娜,李林. 山茱萸环烯醚萜苷对创伤性脑损伤模型大鼠脑内炎性反应反应的影响[J]. 中国临床药理学与治疗学,2010,2010(3):255-259. [8] Ma D, Wang N, Fan X, et al. Protective effects of cornel iridoid glycoside in rats after traumatic brain injury[J]. Neurochem Res, 2018, 43(4):959-971. [9] Tang W J, Ma D L, Yang C C, et al. Cornel iridoid glycoside improves locomotor impairment and decreases spinal cord damage in rats[J]. Biomed Res Int, 2016, 2016:6725381. [10] Feeney D M, Boyeson M G, Linn R T, et al. Responses to cortical injury:I. Methodology and local effects of contusions in the rat[J]. Brain Res, 1981, 211(1):67-77. [11] 马登磊,张兰,李林. 脑外伤动物模型认知障碍评价方法研究进展[J]. 中国康复理论与实践,2015,21(1):65-68. [12] Schmued L C, Hopkins K J. Fluoro-Jade B:a high affinity fluorescent marker for the localization of neuronal degeneration[J]. Brain Res, 2000, 874(2):123-130. [13] Fujimoto S T, Longhi L, Saatman K E, et al. Motor and cognitive function evaluation following experimental traumatic brain injury[J]. Neurosci Biobehav Rev, 2004, 28(4):365-378. [14] Masel B E, DeWitt D S. Traumatic brain injury:a disease process, not an event[J]. J Neurotrauma, 2010, 27(8):1529-1540. [15] Riggio S. Traumatic brain injury and its neurobehavioral sequelae[J]. Neurol Clin, 2011, 29(1):35-47. [16] Stoica B A, Faden A I. Cell death mechanisms and modulation in traumatic brain injury[J]. Neurotherapeutics, 2010, 7(1):3-12. [17] 王建枝,田青. Tau蛋白过度磷酸化机制及其在阿尔茨海默病神经元变性中的作用[J]. 生物化学与生物物理进展,2012, 2012(8):771-777. [18] 马登磊,张旭,罗艺,等. 微管相关蛋白tau转基因细胞和动物模型的建立及tau蛋白病变表征[J]. 首都医科大学学报,2019,40(4):582-587. [19] 杨翠翠,包训杰,张丽,等.山茱萸环烯醚萜苷对APP/PS1/Tau三转基因小鼠脑内病理变化的影响[J].首都医科大学学报,2019,40(4):588-595. [20] 赵子艾. A2AR活化在脑创伤后tau蛋白过度磷酸化及认知障碍中的作用与机制[C].重庆:第三军医大学,2014. [21] Iliff J J, Chen M J, Plog B A, et al. Impairment of glymphatic pathway function promotes tau pathology after traumatic brain injury[J]. J Neurosci, 2014, 34(49):16180-16193. [22] Griesbach G S, Masel B E, Helvie R E, et al. The impact of traumatic brain injury on later life:effects on normal aging and neurodegenerative diseases[J]. J Neurotrauma, 2018, 35(1):17-24. [23] Albayram O, Kondo A, Mannix R, et al. Cis P-tau is induced in clinical and preclinical brain injury and contributes to post-injury sequelae[J]. Nat Commun, 2017, 8(1):1-17. |