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. Author manuscript; available in PMC: 2015 Mar 5.
Published in final edited form as: Neuron. 2014 Mar 5;81(5):1009–1023. doi: 10.1016/j.neuron.2014.01.013

Figure 8. The classical NF-κB pathway mediates microglial activation and MN death.

Figure 8

(A) Model of the mechanism by which SOD1-G93A microglia induce MN death in ALS. The NF-κB pathway is initiated in SOD1-G93A microglia by a SOD1-G93A-dependent mechanism leading to microglial activation and subsequently, MN death via inflammatory pathways. Inhibition of microglial NF-κB in ALS mice blocks microglial activation, down-regulates pro-inflammatory markers, and delays MN death.

(B) Model of IKKβCA mice in which NF-κB is constitutively active only in myeloid cells. Microglia in these mice exhibit a pro-inflammatory phenotype which induces MN death in a mutant SOD1-independent mechanism.