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Nat Neurosci. 2015 Dec;18(12):1725-7. doi: 10.1038/nn.4163. Epub 2015 Nov 9.

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

Author information

1
Institute of Neuroscience, Technische Universität München, Munich, Germany.
2
Department of Psychiatry and Psychotherapy, Technische Universität München, Munich, Germany.
3
Munich Cluster for Systems Neurology (SyNergy), München, Germany.
4
Janelia Farm Research Campus, Howard Hughes Medical Institute, Ashburn, Virginia, USA.
5
Novartis Institute for BioMedical Research, Basel, Switzerland.
6
Department of Cellular Neurology, Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany.

Abstract

Among the most promising approaches for treating Alzheimer's disease is immunotherapy with amyloid-β (Aβ)-targeting antibodies. Using in vivo two-photon imaging in mouse models, we found that two different antibodies to Aβ 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.

PMID:
26551546
DOI:
10.1038/nn.4163
[Indexed for MEDLINE]

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