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 PMID:23184605  

Reducing HDAC6 ameliorates cognitive deficits in a mouse model for Alzheimer's disease.

Nambirajan Govindarajan | Pooja Rao | Susanne Burkhardt | Farahnaz Sananbenesi | Oliver M Schlüter | Frank Bradke | Jianrong Lu | André Fischer
EMBO molecular medicine | 2013

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.

Pubmed ID: 23184605

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VideoMot2 (tool)

RRID:SCR_014334

A video tracking system that takes automated recordings and analyzes animal activity through various arena and maze systems. It can track multiple arenas using one camera, and an unlimited number of zones of interest can be generated for performing spatial analyses or controlling data acquisition. Features include 3-point detection, 3D measurements, access to raw data, and reanalysis of tracking data.

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