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作 者:刘易 丁怡 刘蓉 王建枝[1,3] 柯丹 王小川[1,3] LIU Yi;DING Yi;LIU Rong;WANG Jian-zhi;KE Dan;WANG Xiao-chuan(Department of Pathophysiology,School of Basic Medicine,Tongji Medical College,Huazhong University of Science and Technology,Wuhan 430030,China;Department of Pathophysiology,Weifang Medical University,Weifang 261053,China;Co-innovation Center of Neuroregeneration,Nantong University,Nantong 226001,China)
机构地区:[1]华中科技大学同济医学院基础医学院病理生理学系,湖北武汉430030 [2]潍坊医学院基础医学院病理生理学系,山东潍坊261053 [3]南通大学神经再生协同创新中心,江苏南通226001
出 处:《中国病理生理杂志》2021年第3期538-542,共5页Chinese Journal of Pathophysiology
基 金:国家自然科学基金资助项目(No.31771114)。
摘 要:TBI在全球意外伤害的死亡和伤残原因中居首位,带来了诸多经济、医疗等社会问题。实际上,全世界每年有1000万人死亡和就医直接归因于TBI,大约有5700万人患有脑损伤相关疾病[1]。TBI的幸存者会出现有多种病理现象,例如神经功能缺损,短期和长期脑损伤,认知、行为和情感障碍,所有这些都取决于损伤的严重程度。从功能成像研究中可以明显看出,认知方面的神经系统缺陷是由于海马萎缩和白质束受损所致[2]。TBI可根据其严重程度和作用机制进行分类[3]。在动物模型中,通过复制轻、中、重度不同程度的TBI,观察导致其结果恶化的临床因素对于疾病病理和治疗的理解至关重要。Patients with traumatic brain injury(TBI)are more likely to develop neurodegenerative diseases such as Alzheimer disease(AD)and memory deficits.Asparaginyl endopeptidase(AEP)is a lysosomal cysteine protease,which induces tau protein hyperphosphorylation under brain tissue acidification environment.Moreover,TBI results in increased lactic acid in brain tissue,which promotes the activation of AEP.Nowadays,only a few studies report how TBI,a high risk factor for AD,causes the pathological changes of AD.Therefore,it is particularly important to elucidate the role of AEP,TBI and AD in the pathophysiological process after TBI,so as to provide a theoretical basis for the treatment of neurodegenerative diseases caused by chronic craniocerebral injury.This paper summarizes how AEP affects the occurrence and development of AD after the occurrence of TBI.
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