| Paper: | PS-1A.28 | ||
| Session: | Poster Session 1A | ||
| Location: | H Lichthof | ||
| Session Time: | Saturday, September 14, 16:30 - 19:30 | ||
| Presentation Time: | Saturday, September 14, 16:30 - 19:30 | ||
| Presentation: | Poster | ||
| Publication: | 2019 Conference on Cognitive Computational Neuroscience, 13-16 September 2019, Berlin, Germany | ||
| Paper Title: | Increasing Neurogenesis in Old Mice Rejuvenates Hippocampal Function and Memory | ||
| Manuscript: | Click here to view manuscript | ||
| License: |  This work is licensed under a Creative Commons Attribution 3.0 Unported License. |
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| DOI: | https://doi.org/10.32470/CCN.2019.1147-0 | ||
| Authors: | Federico Calegari, Gabriel Berdugo-Vega, CRTD – Center for Regenerative Therapies Dresden, Technische Universität Dresden, Germany; Gonzalo Arial-Gil, Institute of Biology, Otto-von-Guericke University Magdeburg, Germany; Gerd Kempermann, CRTD – Center for Regenerative Therapies Dresden, Technische Universität Dresden, Germany; Kentaroh Takagaki, Institute of Biology, Otto-von-Guericke University Magdeburg, Germany | ||
| Abstract: | The functional plasticity of the brain decreases during ageing causing marked deficits in contextual learning, allocentric navigation and episodic memory. Adult neurogenesis is a prime example of hippocampal plasticity promoting the contextualization of information but how this influences activity to improve flexible learning is not known. We asked whether a genetically-driven expansion of neural stem cells would compensate the natural decline in neurogenesis and rescue age-dependent deficits on hippocampal physiology and function. We found that neurogenesis promoted the sparsity of memory representations and changed neural activity patterns underlying consolidation. Remarkably, increased neurogenesis also rescued the age-dependent loss in contextual learning, allocentric navigation and episodic memory. Together, our rejuvenation strategy shows that critical aspects of hippocampal physiology can be reversed in old age by exploiting the brain’s endogenous reserve of neural stem cells. | ||