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. 2019 Feb 19;13:1179069519829040. doi: 10.1177/1179069519829040

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© The Author(s) 2019

This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License (http://www.creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https://us.sagepub.com/en-us/nam/open-access-at-sage).

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Figure 3. — Age-related changes in microglia-derived signals negatively affect neurogenic molecular pathways in SVZ NSPCs. In SVZ NSPCs, PI3 kinase (PI3K) promotes AKT kinase activity, which leads to inhibition of the GSK3β kinase. In turn, GSK3β represses the function of β-catenin, which is critical for the neurogenic process. The activities of PI3K and AKT are inhibited by signalling pathways stimulated by reactive microglial cells, which increase during aging. This causes a decrease in the levels of β-catenin and the consequent decline in neurogenesis. Wnt1 ligands released by astrocytes in or near the SVZ niche collaborate to inhibit GSK3β in NSPCs, but Wnt1 expression is negatively affected by reactive microglia-derived signals and hence decreases during aging, contributing to the reduction of neurogenesis. See text for further details.