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Autosomal dominant frontotemporal lobar degeneration due to the C9ORF72 hexanucleotide repeat expansion: late-onset psychotic clinical presentation.常染色体显性遗传额颞叶变性伴 C9ORF72 六核苷酸重复扩展:发病较晚的精神病性临床表现。
Biol Psychiatry. 2013 Sep 1;74(5):384-91. doi: 10.1016/j.biopsych.2013.01.031. Epub 2013 Mar 7.
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Exacerbated inflammatory responses related to activated microglia after traumatic brain injury in progranulin-deficient mice.缺乏颗粒蛋白前体的小鼠创伤性脑损伤后,激活的小胶质细胞引发的炎症反应加剧。
Neuroscience. 2013 Feb 12;231:49-60. doi: 10.1016/j.neuroscience.2012.11.032. Epub 2012 Nov 29.
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Understanding risk factors for Alzheimer's disease: interplay of neuroinflammation, connexin-based communication and oxidative stress.了解阿尔茨海默病的风险因素:神经炎症、连接蛋白通讯和氧化应激的相互作用。
Arch Med Res. 2012 Nov;43(8):632-44. doi: 10.1016/j.arcmed.2012.10.016. Epub 2012 Nov 8.
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Progranulin deficiency promotes neuroinflammation and neuron loss following toxin-induced injury.颗粒蛋白前体缺乏促进毒素诱导损伤后的神经炎症和神经元丢失。
J Clin Invest. 2012 Nov;122(11):3955-9. doi: 10.1172/JCI63113. Epub 2012 Oct 8.
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Frontotemporal lobar degeneration: epidemiology, pathology, diagnosis and management.额颞叶痴呆:流行病学、病理学、诊断与管理。
CNS Drugs. 2012 Oct 1;26(10):841-70. doi: 10.2165/11640070-000000000-00000.
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The genetics and neuropathology of frontotemporal lobar degeneration.额颞叶痴呆的遗传学和神经病理学。
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Transforming growth factor-β stimulates β amyloid uptake by microglia through Smad3-dependent mechanisms.转化生长因子-β通过 Smad3 依赖性机制刺激小胶质细胞摄取β淀粉样蛋白。
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Recent insights into the involvement of progranulin in frontotemporal dementia.近期关于颗粒蛋白前体在额颞叶痴呆中作用的新认识。
Curr Neuropharmacol. 2011 Dec;9(4):632-42. doi: 10.2174/157015911798376361.
10
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先天性免疫系统在阿尔茨海默病和额颞叶痴呆中的作用:聚焦小胶质细胞

The role of the innate immune system in Alzheimer's disease and frontotemporal lobar degeneration: an eye on microglia.

作者信息

Ridolfi Elisa, Barone Cinzia, Scarpini Elio, Galimberti Daniela

机构信息

Neurology Unit, Department of Pathophysiology and Transplantation, University of Milan, Fondazione Cà Granda, IRCCS Ospedale Maggiore Policlinico, Via F. Sforza 35, 20122 Milan, Italy.

出版信息

Clin Dev Immunol. 2013;2013:939786. doi: 10.1155/2013/939786. Epub 2013 Jul 18.

DOI:10.1155/2013/939786
PMID:23970926
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3732611/
Abstract

In the last few years, genetic and biomolecular mechanisms at the basis of Alzheimer's disease (AD) and frontotemporal lobar degeneration (FTLD) have been unraveled. A key role is played by microglia, which represent the immune effector cells in the central nervous system (CNS). They are extremely sensitive to the environmental changes in the brain and are activated in response to several pathologic events within the CNS, including altered neuronal function, infection, injury, and inflammation. While short-term microglial activity has generally a neuroprotective role, chronic activation has been implicated in the pathogenesis of neurodegenerative disorders, including AD and FTLD. In this framework, the purpose of this review is to give an overview of clinical features, genetics, and novel discoveries on biomolecular pathogenic mechanisms at the basis of these two neurodegenerative diseases and to outline current evidence regarding the role played by activated microglia in their pathogenesis.

摘要

在过去几年中,阿尔茨海默病(AD)和额颞叶变性(FTLD)的遗传和生物分子机制已被阐明。小胶质细胞发挥着关键作用,它们是中枢神经系统(CNS)中的免疫效应细胞。它们对大脑中的环境变化极为敏感,并在中枢神经系统内发生的多种病理事件(包括神经元功能改变、感染、损伤和炎症)的刺激下被激活。虽然短期的小胶质细胞活动通常具有神经保护作用,但慢性激活已被认为与神经退行性疾病(包括AD和FTLD)的发病机制有关。在此框架下,本综述的目的是概述这两种神经退行性疾病的临床特征、遗传学以及生物分子致病机制的新发现,并概述关于活化小胶质细胞在其发病机制中所起作用的现有证据。