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. 2019 Nov 15;16:225. doi: 10.1186/s12974-019-1621-2

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© The Author(s). 2019

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided 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 Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Fig. 5 — Proposed model for synaptamide/GPR110-mediated suppression of LPS-induced neuroinflammation. LPS induces activation of peripheral immune cells such as neutrophils and macrophages, which increases the level of pro-inflammatory mediators. Under systemic inflammatory conditions, inflammatory molecules produced by peripheral immune cells traverse the blood-brain barrier and activate microglia causing neuroinflammation. Pharmacologically administered synaptamide acts on central and peripheral targets where GPR110 is expressed or induced after LPS challenge to ameliorate neuroinflammation through cAMP-dependent immune regulatory mechanisms. Synaptamide endogenously produced from DHA in the brain or peripheral tissues can also be protective