Decreased amyloid-β and increased neuronal hyperactivity by immunotherapy in Alzheimer's models

被引：110
作者：
Busche, Marc Aurel [1 ,2 ,3 ]
Grienberger, Christine [1 ,4 ]
Keskin, Aylin D. [1 ]
Song, Beomjong [1 ]
Neumann, Ulf [5 ]
Staufenbiel, Matthias [6 ]
Foerstl, Hans [2 ]
Konnerth, Arthur [1 ,3 ]
机构：
[1] Tech Univ Munich, Inst Neurosci, D-80290 Munich, Germany
[2] Tech Univ Munich, Dept Psychiat & Psychotherapy, D-80290 Munich, Germany
[3] Munich Cluster Syst Neurol SyNergy, Munich, Germany
[4] Howard Hughes Med Inst, Janelia Farm Res Campus, Ashburn, VA USA
[5] Novartis Inst BioMed Res, Basel, Switzerland
[6] Univ Tubingen, Hertie Inst Clin Brain Res, Dept Cellular Neurol, Tubingen, Germany
来源：
NATURE NEUROSCIENCE | 2015年 / 18卷 / 12期
关键词：
MOUSE MODEL; DISEASE; ANTIBODIES; PATHOLOGY; SEIZURES; TRIALS;
D O I：
10.1038/nn.4163
中图分类号：
Q189 [神经科学];
学科分类号：
071006 ;
摘要：
Among the most promising approaches for treating Alzheimer's disease is immunotherapy with amyloid-beta (A beta)-targeting antibodies. Using in vivo two-photon imaging in mouse models, we found that two different antibodies to A beta used for treatment were ineffective at repairing neuronal dysfunction and caused an increase in cortical hyperactivity. This unexpected finding provides a possible cellular explanation for the lack of cognitive improvement by immunotherapy in human studies.
引用
收藏
页码：1725 / 1727
页数：3
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