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

Immunotherapy with antibodies targeting the amyloid-β peptide has yet to show any cognitive benefit in Alzheimer's disease patients in clinical trials. In vivo two-photon imaging in mouse models of Alzheimer's disease now reveals that these antibodies do not alleviate neuronal dysfunction...

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Veröffentlicht in:	Nature neuroscience 2015-12, Vol.18 (12), p.1725-1727
Hauptverfasser:	Busche, Marc Aurel, Grienberger, Christine, Keskin, Aylin D, Song, Beomjong, Neumann, Ulf, Staufenbiel, Matthias, Förstl, Hans, Konnerth, Arthur
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Sprache:	eng
Schlagworte:	14/69 631/378/1689/1283 692/699/375/132 Alzheimer Disease - immunology Alzheimer Disease - metabolism Alzheimer Disease - therapy Alzheimer's disease Amyloid beta-Peptides - immunology Amyloid beta-Peptides - metabolism Amyloid beta-protein Animal Genetics and Genomics Animals Behavioral Sciences Biological Techniques Biomedicine brief-communication Development and progression Female Genetic aspects Health aspects Humans Immunotherapy Immunotherapy - methods Methods Mice Mice, Transgenic Neural circuitry Neurobiology Neurons - immunology Neurons - metabolism Neurosciences Patient outcomes Properties
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container_title	Nature neuroscience
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creator	Busche, Marc Aurel Grienberger, Christine Keskin, Aylin D Song, Beomjong Neumann, Ulf Staufenbiel, Matthias Förstl, Hans Konnerth, Arthur
description	Immunotherapy with antibodies targeting the amyloid-β peptide has yet to show any cognitive benefit in Alzheimer's disease patients in clinical trials. In vivo two-photon imaging in mouse models of Alzheimer's disease now reveals that these antibodies do not alleviate neuronal dysfunction and can even worsen it. 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.
doi_str_mv	10.1038/nn.4163
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subjects	14/69 631/378/1689/1283 692/699/375/132 Alzheimer Disease - immunology Alzheimer Disease - metabolism Alzheimer Disease - therapy Alzheimer's disease Amyloid beta-Peptides - immunology Amyloid beta-Peptides - metabolism Amyloid beta-protein Animal Genetics and Genomics Animals Behavioral Sciences Biological Techniques Biomedicine brief-communication Development and progression Female Genetic aspects Health aspects Humans Immunotherapy Immunotherapy - methods Methods Mice Mice, Transgenic Neural circuitry Neurobiology Neurons - immunology Neurons - metabolism Neurosciences Patient outcomes Properties
title	Decreased amyloid-β and increased neuronal hyperactivity by immunotherapy in Alzheimer's models
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