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. 2021 May 5;99(8):1033–1042. doi: 10.1007/s00109-021-02080-4

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© The Author(s) 2021

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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 2 — a Ligand binding to surface receptor (e.g. EGF-R) evokes downstream signaling leading to MAPK^ERK activation. b The introduction of BRAF^V600E in mouse microglia leads to substantial overactivation of MAPK^ERK. This resulted in clinical and histopathological substantial neurodegeneration. c Early administration of BRAF^V600E-inhibiting PLX4720 to these mice with BRAF^V600E expressing microglia gave diminished MAPK^ERK activation in these microglia and clinically as well as histopathologically attenuated neurodegeneration [5]