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. 2017 Apr 28;7:1277. doi: 10.1038/s41598-017-01215-3

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© The Author(s) 2017

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Mechanisms synopsis. Cartoon illustrating the concept that CaSR-dependent signalling can deeply affect the balance between hAPP NAP and AP and hence play a role in the promotion or prevention of AD development. Left panel. The main mechanisms by which Aβ_25–35 alone (top) or +CMT (bottom) alters the hAPP physiological NAP in favour of AP. Right panel. The main mechanisms by which calcilytic NPS 2143 restores the hAPP NAP while hindering the AP in Aβ_25–35-exposed adult human astrocytes either in absence (top) or in the presence of CMT (bottom). The emojis indicate what most likely happens to the neurons exposed to the various agents (human astrocytes survive). See the text for further details.