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. 2022 Feb 26;12:83. doi: 10.1038/s41398-022-01788-2

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© The Author(s) 2022

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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Fig. 8 — 1 It is plausible that exposure to obesogenic diets rich in saturated fatty acids (SFAs) increase TACE/ADAM17 sheddase expression and activities, (2) leading to dysregulation of neuroinflammatory (e.g., tumor necrosis factor alfa, TNF-α) and neurodevelopmental (ErbB4) mediators. (3) TNF receptor (TNFR) activation and prolonged ErbB4 cleavage tip the inflammatory balance to a pro-inflammatory state associated with microglial activation. (4) Neuroinflammation and microglial activation promote synaptic pruning and remodeling. (5) Disruption in microglia-synapse interactions contributes to synapse loss, dysfunction, and, consequently, hippocampal volume atrophy. (6) In summary, evidence in this study supports the conclusion that microglia respond to trophic factors and secrete cytokines, which are critical for normative synaptic plasticity in the maturing brain [137, 138]. Our data suggest that an imbalance in the levels of cytokines and neurotrophic factors during early pre-obesity states can impair microglia, synaptic plasticity, which may result in anxiety. Although our analyses focused on microglia and provided limited directionality of the effects, this dataset provides a rich resource for identifying meaningful synaptic targets in response to an obesogenic WD.