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寻找治疗阿尔茨海默病的方法及潜在的免疫抑制治疗干预措施。

In search of a treatment for Alzheimer's disease and potential immunonosuppresive therapeutic interventions.

作者信息

Dhawan Naveen, Puangco Jay, Jandial Rahul

机构信息

UCLA Department of Medicine, CA, USA.

出版信息

Neuro Endocrinol Lett. 2008 Aug;29(4):410-20.

PMID:18766151
Abstract

Alzheimer's disease (AD) is a serious neurodegenerative disease of aging. Recent projections of the dramatic increase in AD incidence worldwide by 2050 reveal its magnitude as a world-wide health crisis and underscore the urgent need to understand the etiology of AD in order to develop therapeutic interventions. A popular debate among scientists has traditionally pitted those in support of Beta amyloid protein as a causative factor ("Baptists") against others who implicate tau hyperphosphorylation ("Tauists"). Considering the significance of Beta amyloid protein and hyperphosphorlyated tau protein aggregates in AD pathology, this article delves into the nature of inflammation associated with these aggregates. Aspects of inflammation focus on microglia, resident immune cells of the CNS that are activated during AD inflammation and are known to play a significant role in pathogenesis. This article discusses the role of microglia, inflammation, and the immune response as a middle ground in the debate between the "Tauists" and the "Baptists" respective positions. It explores recent advances in immunotherapy and supports continued research in and use of immunosuppressive regimens as potential therapeutic interventions for AD.

摘要

阿尔茨海默病(AD)是一种严重的衰老性神经退行性疾病。近期对到2050年全球AD发病率急剧上升的预测揭示了其作为全球健康危机的严重程度,并强调迫切需要了解AD的病因以开发治疗干预措施。传统上,科学家之间的一场热门辩论使支持β淀粉样蛋白作为致病因素的一方(“浸礼会派”)与那些认为tau蛋白过度磷酸化是病因的另一方(“tau派”)针锋相对。鉴于β淀粉样蛋白和过度磷酸化的tau蛋白聚集体在AD病理学中的重要性,本文深入探讨了与这些聚集体相关的炎症的本质。炎症方面聚焦于小胶质细胞,它是中枢神经系统的常驻免疫细胞,在AD炎症期间被激活,并且已知在发病机制中起重要作用。本文讨论了小胶质细胞、炎症和免疫反应在“tau派”和“浸礼会派”各自立场的辩论中作为中间立场的作用。它探讨了免疫疗法的最新进展,并支持继续研究和使用免疫抑制方案作为AD的潜在治疗干预措施。

相似文献

1
In search of a treatment for Alzheimer's disease and potential immunonosuppresive therapeutic interventions.寻找治疗阿尔茨海默病的方法及潜在的免疫抑制治疗干预措施。
Neuro Endocrinol Lett. 2008 Aug;29(4):410-20.
2
Microglia as a potential bridge between the amyloid beta-peptide and tau.小胶质细胞作为淀粉样β肽和tau蛋白之间的潜在桥梁。
Ann N Y Acad Sci. 2004 Dec;1035:85-103. doi: 10.1196/annals.1332.006.
3
Microglial interaction with beta-amyloid: implications for the pathogenesis of Alzheimer's disease.小胶质细胞与β-淀粉样蛋白的相互作用:对阿尔茨海默病发病机制的影响。
Microsc Res Tech. 2001 Jul 15;54(2):59-70. doi: 10.1002/jemt.1121.
4
[Therapy of Alzheimer disease].[阿尔茨海默病的治疗]
Neuropsychopharmacol Hung. 2009 Mar;11(1):27-33.
5
[Fundamental data on the pathologies amyloid and Tau in Alzheimer's disease: which therapeutic perspectives?].[阿尔茨海默病中淀粉样蛋白和 Tau 蛋白病变的基础数据:有哪些治疗前景?]
Ann Pharm Fr. 2009 Mar;67(2):136-53. doi: 10.1016/j.pharma.2009.01.002. Epub 2009 Feb 28.
6
The role of inflammation in Alzheimer's disease.炎症在阿尔茨海默病中的作用。
Int J Biochem Cell Biol. 2005 Feb;37(2):289-305. doi: 10.1016/j.biocel.2004.07.009.
7
Clinical aspects of inflammation in Alzheimer's disease.阿尔茨海默病炎症的临床方面
Int Rev Psychiatry. 2005 Dec;17(6):503-14. doi: 10.1080/02646830500382037.
8
Progress in Alzheimer's disease drug discovery: an update.阿尔茨海默病药物研发进展:最新情况
Curr Opin Investig Drugs. 2009 Jan;10(1):23-34.
9
Inflammation and Alzheimer's disease.炎症与阿尔茨海默病
Int J Clin Pract. 2003 Jan-Feb;57(1):36-9.
10
Inflammatory processes in Alzheimer's disease.阿尔茨海默病中的炎症过程。
Prog Neuropsychopharmacol Biol Psychiatry. 2003 Aug;27(5):741-9. doi: 10.1016/S0278-5846(03)00124-6.

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