TDP-43与神经退行性疾病及脑损伤的相关性研究进展

蔡斌; 宋海; 王振; 韩雪; 于建云

TDP-43与神经退行性疾病及脑损伤的相关性研究进展

蔡斌¹,
宋海^1,2,
王振¹,
韩雪¹,
于建云¹

1. 昆明医科大学法医学院
2. 昆明医科大学第一附属医院神经外科

基金项目:

基金：国家自然科学基金资助项目 (81360467); 云南省科技厅-昆明医科大学应用基础研究联合专项基金资助项目 (2013FB104);

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出版历程
- 收稿日期: 2017-09-10

Research Progress of the Relationship of the Expression of TAR DNA/RNA-binding Domain Protein 43 in Neurodegenerative Disease and Brain Injury

Cai Bin ¹,
Song Hai ^1,2,
Wang Zhen ¹,
Han Xue ¹,
Yu Jian Yun ¹

Funds:

基金：国家自然科学基金资助项目 (81360467); 云南省科技厅-昆明医科大学应用基础研究联合专项基金资助项目 (2013FB104);

摘要

摘要: TAR DNA/RNA结合蛋白43 (TARDNA/RNA-binding domain protein 43, TDP-43) 是一种高度保守、广泛表达的核蛋白.肌萎缩侧索硬化症 (amyotrophic lateral sclerosis, ALS) 、额颞叶变性 (frontotemporal lobar degeneration, FTLD) 、阿尔茨海默病 (alzheimer disease, AD) 等神经退行性疾病的病理学标记蛋白被公认是TDP-43.就TDP-43的结构、功能及其与神经退行性疾病之间的关系作一综述.同时在对TDP-43生物学特性认识的基础上, 探讨TDP-43在急、慢性颅脑损伤中的特殊表达与作用, 从而探索TDP-43在法医病理学中确定死亡原因、判定致伤致残情况的可行性.
- TDP-43 /
- 神经退行性疾病 /
- 法医病理学 /
- 脑损伤
Abstract: TAR DNA/RNA-binding domain protein 43 (TDP-43) is a highly conserved and widely expressed nuclear protein. TDP-43 is recognized as a pathological marker protein of amyotrophic lateral sclerosis (ALS) , frontotemporal lobar degeneration (FTLD) and alzheimer disease (AD) .This article discusses the structure and the function of TDP-43 and the relationship of its expression in neurodegenerative disease.Meanwhile, this article emphatically probes into the specific expression andfunction of TDP-43 in acute and chronic brain injury based on the knowledge of its biological characteristics, aiming to explore the feasibility for determining the cause of death and the injury and disability situations by TDP-43 in forensic pathology.
- TDP-43 /
- Neurodegenerative disease /
- Forensic pathology /
- Brain injuries

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参考文献(24)

[1]	[1]NEUMANN M, SAMPATHU D M, KWONG L K, et al.Ubiquitinated TDP-43 in frontotemporal lobar degeneration and amy-otrophic lateral sclerosis[J].Science, 2006, 314 (5796) :130-133.
[2]	[2]JOSEPHS K A, MURRAY M E, WHITWELL J L, et al.Staging TDP-43 pathology in Alzheimer’s disease[J].Acta Neuropathol, 2014, 127 (3) :441-450.
[3]	[3]BURATTI E, BARALLE F E.Multiple roles of TDP-43 in gene expression, splicing regulation, and human disease[J].Front Biosci, 2008, (13) :867-878.
[4]	[4]ZHANG Y J, XU Y F, COOK C, et al.Aberrant cleavage of TDP-43 enhances aggregation and cellular toxicity[J].Proc Natl Acad Sci U S A, 2009, 106 (18) :7607-7612.
[5]	[5]AYALA Y M, MISTELI T, BARALLE FE.TDP-43regulates retinoblastoma protein phosphorylation through the repression of cyclin-dependent kinase 6 expression[J].Proc Natl Acad Sci USA, 2008, 105 (10) :3785-3789.
[6]	[6]FIESEL F C, VOIGT A, WEBER S S, et al.Knockdown of transactive response DNA-binding protein (TDP-43) downregulates histone deacetylase 6[J].EMBO J, 2010, 29 (1) :209-221.
[7]石磊, 叶城辉, 何若洁.肌萎缩侧索硬化症基因TDP-43致病突变对斑马鱼毒性的影响[J].中山大学学报, 2014, 35 (4) :481-487.
[8]	[8]PHOEBE S, TSOI D R, KYOUNG-JAE CHOI, et al.The N-terminal domain of ALS-linked TDP-43 assembles without Misfolding[J].Angewandte Chemie International Edition, 2017, 56 (47) :12590-12593.
[9]赵嘉玲, 樊东升.外周组织中的TDP-43蛋白病理及其临床诊断价值研究进展[J].北京医学, 2016, 38 (5) :474-477.
[10]	[10]MACKENZIE I R, BABORIE A, PICKERING-BROWN S, et al.Het-erogeneity of ubiquitin pathology in frontotemporal lobardegeneration:classification and relation to clinical phenotype[J].Acta Neuropathol, 2006, 112 (5) :539-549.
[11]	[11]DAVIDSON Y, KELLEY T, MACKENZIE I R, et al.Ubiq-uitinated pathological lesions in frontotemporal lobardegeneration contain the TAR DNA-binding protein, TDP-43[J].Acta Neuropathol, 2007, 113 (5) :521-533.
[12]	[12]RACHEL H, TAN, JILLIAN J, et al.TDP-43 proteinopathies:pathological identification of brain regions differentiating clinical phenotypes[J].Brain, 2015, 138, (5) :3110-3122,
[13]	[13]EMMA L, SCOTTER, HAN-JOU CHEN, et al.TDP-43proteinopathy and ALS:insights into disease mechanisms and therapeutic targets, Neurotherapeutics[J].April, 2015, 12 (2) :352-363.
[14]	[14]EMMA L, SCOTTER, CAROLINE VANCE, et al.Differential roles of the ubiquitin proteasome system and autophagy in the clearance of soluble and aggregated TDP-43 species[J].Journal of Cell Science, 2014, 127 (6) :1263-1278.
[15]	[15]URYU K, NAKASHIMA-YASUDA H, FORMAN M S, et al.Concomitant TAR-DNA-binding protein 43 pathology is present in Alzheimer disease and corticobasal degenerationbut not in other tauopathies[J].J Neuropathol Exp Neurol, 2008, 67 (6) :555-564.
[16]	[16]DUYCKAERTS C, DELATOUR B, POTIER MC.Classification and basic pathology of Alzheimer disease[J].Acta Neuropathol, 2009, 118 (1) :5-36.
[17]	[17]KEITH A JOSEPHS, DENNIS W DICKSON, et al.Rates of hippocampal atrophy and presence of post-mortem TDP-43 in patients with Alzheimer's disease:a longitudinal retrospective study[J].The Lancet Neurology, 2017, 16 (11) :917-924.
[18]	[18]KEITH A, JOSEPHS, DENNIS W, et al.TDP-43 drives faster rates of hippocampal atrophy in Alzheimer’s disease starting at least 10 years prior to death[J].Alzheimer’s and Denmentia, 2017, 13 (7) :1553-1562.
[19]彭敏.创伤性脑外伤大鼠海马中TDP-43及PGRN蛋白表达的研究[D].长沙:中南大学硕士论文, 2013.
[20]	[20]BRANDON PETER LUCKE-WOLD, RYAN CODDINGTON TURNER, ARIC FLINT LOGSDON, et al.Linking traumatic brain injury to chronic traumatic encephalopathy:Identification of potential mechanisms leading to neurofibrillary tangle development[J].Journal of Neurotrauma, 2014, 31 (13) :1129-1138.
[21]	[21]KIMBRA KENNEY, DIEGO IACONO, BRIAN L EDLOW, et al.Dementia after moderate-severe traumatic brain injury:Coexistence of multiple proteinopathies[J].Journal of Neuropathology&Experimental Neurology, 2018, 77 (1) :50-63,
[22]	[22]JESSICA N, SAYKALLY, WHITNEY A, et al.Repetitive mild closed head injury alters protein expression and dendritic complexity in a mouse model[J].Journal of Neurotrauma[J].January, 2018, 35 (1) :139-148.
[23]	[23]ALAN I, FADEN, DAVID J, et al.Chronic Neurodegeneration after traumatic brain injury:Alzheimer disease, chronic traumatic encephalopathy, or persistent neuroinflammation[J].Neurotherapeutics, 2015, 12 (1) :143-150.
[24]张睿, 郑永江, 蔡斌.迷迭香干预三重脑震荡大鼠焦虑行为变化[J].昆明医科大学学报, 2017, 38 (8) :11-15.

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