Neuroinflammation as motor of Alzheimer's disease

被引:7
|
作者
Castro-Gomez, Sergio [1 ]
Binder, Julius [1 ]
Heneka, Michael T. [1 ,2 ]
机构
[1] Univ Klinikum Bonn AoR, Klin Neurodegenerat Erkrankungen & Gerontopsychia, Sigmund Freud Str 25,Venusberg Campus 1, D-53127 Bonn, Germany
[2] Deutsch Zentrum Neurodegenerat Erkrankungen, Bonn, Germany
来源
NERVENARZT | 2019年 / 90卷 / 09期
关键词
Cerebral immune system; Neurodegeneration; Microglia; Dementia; Genetic risk factors; EXACERBATES TAU PATHOLOGY; GENOME-WIDE ASSOCIATION; AMYLOID-BETA; TRANSLOCATOR PROTEIN; IDENTIFIES VARIANTS; MICROGLIA; EXPRESSION; BRAIN; RISK; PROLIFERATION;
D O I
10.1007/s00115-019-0778-3
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Sporadic Alzheimer's disease is the most common neurodegenerative disorder and represents a very important public healthcare problem with a devastating economic burden for industrialized countries. Recent knowledge acquired from experimental, epidemiological, radiological and genome-wide association studies (GWAS) underline the role of the innate immune system in the pathophysiology of this disease. This article reviews and discusses the function of the cerebral innate immune system, the newly discovered genes associated with the disease development and the experimental evidence around the role of microglia in the onset and progression of Alzheimer's disease. The discovery of different microglia phenotypes associated with the pathology as well as new molecular players will enable the development of new preventive and therapeutic strategies by modulating neuroinflammation in neurodegenerative diseases.
引用
收藏
页码:898 / 906
页数:9
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