Microglial Cx3cr1 knockout prevents neuron loss in a mouse model of Alzheimer's disease

被引：420

作者：

Fuhrmann, Martin ^{[1
]}

Bittner, Tobias ^{[1
]}

Jung, Christian K. E. ^{[1
]}

Burgold, Steffen ^{[1
]}

Page, Richard M. ^{[2
]}

Mitteregger, Gerda ^{[1
]}

Haass, Christian ^{[2
]}

LaFerla, Frank M. ^{[3
]}

Kretzschmar, Hans ^{[1
]}

Herms, Jochen ^{[1
]}

机构：

[1] Univ Munich, Ctr Neuropathol & Prion Res, Munich, Germany

[2] Univ Munich, German Ctr Neurodegenerat Dis Munich, Munich, Germany

[3] Univ Calif Irvine, Dept Neurobiol & Behav, Irvine, CA USA

来源：

NATURE NEUROSCIENCE | 2010年 / 13卷 / 04期

关键词：

FRACTALKINE-RECEPTOR; BRAIN-DAMAGE; IN-VIVO; BETA; INFLAMMATION; MAINTENANCE; PLAQUES; CELLS;

D O I：

10.1038/nn.2511

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Microglia, the immune cells of the brain, can have a beneficial effect in Alzheimer's disease by phagocytosing amyloid-beta. Two-photon in vivo imaging of neuron loss in the intact brain of living Alzheimer's disease mice revealed an involvement of microglia in neuron elimination, indicated by locally increased number and migration velocity of microglia around lost neurons. Knockout of the microglial chemokine receptor Cx3cr1, which is critical in neuron-microglia communication, prevented neuron loss.

引用

页码：411 / 413

页数：3

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