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. 2017 Aug 8;9:270. doi: 10.3389/fnagi.2017.00270

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Copyright © 2017 Zhao, Jiang, Zhang, Zhang, Ding and Ji.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Main biological mechanisms of PSD and how RIC plays its roles in preventing PSD. HPA indicates hypothalamic-pituitary-adrenal; PSD, post-stroke depression; RIC, remote ischemic conditioning. Stroke leads to PSD through several biological mechanisms, such as the ascending monoamine systems, the abnormality of HPA axis, the alteration of neuroplasticity and inflammation. Inflammation also has complex interactions with monoamine systems, HPA axis and neuroplasticity. RIC can prevent PSD through anti-inflammation and other underlying mechanisms directly, and it has effects on monoamine systems, HPA axis and neuroplasticity indirectly. All these effects of RIC could be the potential pathways to prevent and treat PSD.