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[抗N-甲基-D-天冬氨酸受体脑炎发病机制的研究进展]

[Research advances in pathogenesis of anti-N-methyl-D-aspartate receptor encephalitis].

作者信息

Liu Meng-Jia, Zou Li-Ping

机构信息

Children's Medical Center, General Hospital of People's Liberation Army, Beijing 100853, China.

出版信息

Zhongguo Dang Dai Er Ke Za Zhi. 2014 Jun;16(6):571-4.

PMID:24927429
Abstract

Anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis is the most prevalent type of encephalitis. Investigating the pathogenesis of anti-NMDAR encephalitis will enhance our understanding of this disease and play a central part in providing reasonable treatment for the patients. The pathogenesis is elucidated as follows: (1) the findings of the relationship between anti-NMDAR encephalitis and tumors; (2) further research on the relationship between anti-NMDAR encephalitis and tumors; (3) NMDAR epitopes and the autoimmunity of patients; (4) the interaction between antibody and NMDAR; (5) the pathogenesis of anti-NMDAR encephalitis without tumors. This review gives a brief introduction to the methodology and way of finding out the valuable clinical problems and making a clear and explicit explanation of them by exhibiting the process of discovering the disease, disclosing its relationship with tumors, and investigating its pathological and molecular mechanism. Current studies have demonstrated that anti-NMDAR encephalitis is an autoimmune disease of the nervous system that is closely associated with tumors, particularly ovarian teratoma.

摘要

抗N-甲基-D-天冬氨酸受体(NMDAR)脑炎是最常见的脑炎类型。研究抗NMDAR脑炎的发病机制将增进我们对该疾病的了解,并在为患者提供合理治疗方面发挥核心作用。其发病机制阐述如下:(1)抗NMDAR脑炎与肿瘤之间关系的研究结果;(2)对抗NMDAR脑炎与肿瘤之间关系的进一步研究;(3)NMDAR表位与患者自身免疫性;(4)抗体与NMDAR之间的相互作用;(5)无肿瘤的抗NMDAR脑炎的发病机制。本综述通过展示发现该疾病的过程、揭示其与肿瘤的关系以及研究其病理和分子机制,简要介绍了找出有价值的临床问题并对其进行清晰明确解释的方法和途径。目前的研究表明,抗NMDAR脑炎是一种与肿瘤尤其是卵巢畸胎瘤密切相关的神经系统自身免疫性疾病。

相似文献

1
[Research advances in pathogenesis of anti-N-methyl-D-aspartate receptor encephalitis].[抗N-甲基-D-天冬氨酸受体脑炎发病机制的研究进展]
Zhongguo Dang Dai Er Ke Za Zhi. 2014 Jun;16(6):571-4.
2
The N-methyl-D-aspartate receptor, a precursor to N-methyl-D-aspartate receptor encephalitis, is found in the squamous tissue of ovarian teratomas.N-甲基-D-天冬氨酸受体是N-甲基-D-天冬氨酸受体脑炎的前身,存在于卵巢畸胎瘤的鳞状组织中。
Int J Gynecol Pathol. 2014 Nov;33(6):598-606. doi: 10.1097/PGP.0000000000000104.
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Abnormal neurons in teratomas in NMDAR encephalitis.NMDAR 脑炎性畸胎瘤中的异常神经元。
JAMA Neurol. 2014 Jun;71(6):717-24. doi: 10.1001/jamaneurol.2014.488.
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Immunopathological significance of ovarian teratoma in patients with anti-N-methyl-d-aspartate receptor encephalitis.抗 N-甲基-D-天冬氨酸受体脑炎患者卵巢畸胎瘤的免疫病理学意义。
Eur Neurol. 2014;71(1-2):42-8. doi: 10.1159/000353982. Epub 2013 Nov 27.
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Does MAP2 have a role in predicting the development of anti-NMDAR encephalitis associated with benign ovarian teratoma? A report of six new pediatric cases.微管相关蛋白2(MAP2)在预测与良性卵巢畸胎瘤相关的抗N-甲基-D-天冬氨酸受体(NMDAR)脑炎的发展中是否起作用?6例新的儿科病例报告。
Pediatr Dev Pathol. 2015 Mar-Apr;18(2):122-6. doi: 10.2350/14-09-1554-OA.1. Epub 2015 Jan 8.
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Anti-N-methyl-D-aspartate receptor encephalitis associated with an ovarian teratoma: two cases report and anesthesia considerations.与卵巢畸胎瘤相关的抗N-甲基-D-天冬氨酸受体脑炎:两例报告及麻醉注意事项
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[Ovarian teratoma associated with anti-N-methyl-D-aspartate receptor encephalitis: a report of 5 cases and review of the literature].[卵巢畸胎瘤合并抗N-甲基-D-天冬氨酸受体脑炎:5例报告并文献复习]
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Ovarian teratoma associated with anti-N-methyl D-aspartate receptor encephalitis: a report of 5 cases documenting prominent intratumoral lymphoid infiltrates.抗 N-甲基-D-天冬氨酸受体脑炎相关的卵巢畸胎瘤:5 例伴显著肿瘤内淋巴样浸润的病例报告。
Int J Gynecol Pathol. 2012 Sep;31(5):429-37. doi: 10.1097/PGP.0b013e31824a1de2.
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[Anti-nMDA receptor encephalitis--clinical manifestations and pathophysiology].[抗N-甲基-D-天冬氨酸受体脑炎——临床表现与病理生理学]
Brain Nerve. 2008 Sep;60(9):1047-60.
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[Etiology of anti-N-methyl-D-aspartate receptor encephalitis].[抗N-甲基-D-天冬氨酸受体脑炎的病因]
Zhongguo Dang Dai Er Ke Za Zhi. 2014 Jun;16(6):567-70.

引用本文的文献

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[Clinical analysis of anti-NMDA receptor encephalitis complicated by paroxysmal sympathetic hyperactivity].抗N-甲基-D-天冬氨酸受体脑炎合并阵发性交感神经过度兴奋的临床分析
Zhongguo Dang Dai Er Ke Za Zhi. 2016 Apr;18(4):376-8. doi: 10.7499/j.issn.1008-8830.2016.04.019.