Reducing HDAC6 ameliorates cognitive deficits in a mouse model for Alzheimer's disease
Abstract: Histone deacetylases (HDACs) are currently being discussed as promising therapeutic targets to treat neurodegenerative diseases. However, the role of specific HDACs in cognition and neurodegeneration remains poorly understood. Here, we investigate the function of HDAC6, a class II member of the HDAC superfamily, in the adult mouse brain. We report that mice lacking HDAC6 are cognitively normal but reducing endogenous HDAC6 levels restores learning and memory and α‐tubulin acetylation in a mouse model for Alzheimer's disease (AD). Our data suggest that this therapeutic effect is, at least in part, linked to the observation that loss of HDAC6 renders neurons resistant to amyloid‐β‐mediated impairment of mitochondrial trafficking. Thus, our study suggests that targeting HDAC6 could be a suitable strategy to ameliorate cognitive decline observed in AD.
- Location
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Deutsche Nationalbibliothek Frankfurt am Main
- Extent
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Online-Ressource
- Language
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Englisch
- Bibliographic citation
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Reducing HDAC6 ameliorates cognitive deficits in a mouse model for Alzheimer's disease ; volume:5 ; number:1 ; year:2013 ; pages:52-63 ; extent:12
EMBO molecular medicine / European Molecular Biology Organization ; 5, Heft 1 (2013), 52-63 (gesamt 12)
- Creator
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Govindarajan, Nambirajan
Rao, Pooja
Burkhardt, Susanne
Sananbenesi, Farahnaz
Schlüter, Oliver M.
Bradke, Frank
Lu, Jianrong
Fischer, André
- DOI
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10.1002/emmm.201201923
- URN
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urn:nbn:de:101:1-2023020607380384482086
- Rights
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Open Access; Der Zugriff auf das Objekt ist unbeschränkt möglich.
- Last update
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14.08.2025, 10:48 AM CEST
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Associated
- Govindarajan, Nambirajan
- Rao, Pooja
- Burkhardt, Susanne
- Sananbenesi, Farahnaz
- Schlüter, Oliver M.
- Bradke, Frank
- Lu, Jianrong
- Fischer, André
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