Physical activity delays hippocampal neurodegeneration and rescues memory deficits in an Alzheimer disease mouse model
2016 | journal article. A publication with affiliation to the University of Göttingen.
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Physical activity delays hippocampal neurodegeneration and rescues memory deficits in an Alzheimer disease mouse model
Hüttenrauch, M. ; Brauß, A.; Kurdakova, A.; Borgers, H.; Klinker, F. ; Liebetanz, D. & Salinas-Riester, G. et al. (2016)
Translational Psychiatry, 6(5) art. e800. DOI: https://doi.org/10.1038/tp.2016.65
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- Authors
- Hüttenrauch, M. ; Brauß, A.; Kurdakova, A.; Borgers, H.; Klinker, Florian ; Liebetanz, David ; Salinas-Riester, G. ; Wiltfang, Jens ; Klafki, Hans-Wolfgang ; Wirths, Oliver
- Abstract
- The evidence for a protective role of physical activity on the risk and progression of Alzheimer’s disease (AD) has been growing in the last years. Here we studied the influence of a prolonged physical and cognitive stimulation on neurodegeneration, with special emphasis on hippocampal neuron loss and associated behavioral impairment in the Tg4-42 mouse model of AD. Tg4-42 mice overexpress Aβ4-42 without any mutations, and develop an age-dependent hippocampal neuron loss associated with a severe memory decline. We demonstrate that long-term voluntary exercise diminishes CA1 neuron loss and completely rescues spatial memory deficits in different experimental settings. This was accompanied by changes in the gene expression profile of Tg4-42 mice. Deep sequencing analysis revealed an upregulation of chaperones involved in endoplasmatic reticulum protein processing, which might be intimately linked to the beneficial effects seen upon long-term exercise. We believe that we provide evidence for the first time that enhanced physical activity counteracts neuron loss and behavioral deficits in a transgenic AD mouse model. The present findings underscore the relevance of increased physical activity as a potential strategy in the prevention of dementia.
- Issue Date
- 2016
- Journal
- Translational Psychiatry
- ISSN
- 2158-3188
- Language
- English
- Sponsor
- Open-Access Publikationsfonds 2016
Open-Access-Publikationsfonds 2016