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Fig. 8 | Acta Neuropathologica Communications

Fig. 8

From: Neuronal dysfunction caused by FUSR521G promotes ALS-associated phenotypes that are attenuated by NF-κB inhibition

Fig. 8

Inhibition of NF-κB with IMS-088 restores dendritic mitochondrial stasis in neurons expressing FUSR521G. a Primary cortical neurons cultured from hFUSR521G/Meox (FUSR521G) or littermate control (CTL) mice treated with vehicle (veh) or IMS-088 co-stained with anti-acetylated P65 (acP65), anti-MAP2 (dendritic marker) and DAPI show IMS-088 blocks the activation and nuclear localisation of acP65 in neurons expressing FUSR521G. b Neuron cultures co-stained with Mitotracker, anti-MAP2 and DAPI. c Treatment with IMS-088 promotes an increase in the number of mitochondria within the dendrites of neurons expressing FUSR521G. d Live images of neurons stained with tetramethylrhodamine, methyl ester (TMRM). e Treatment with IMS-088 promotes an increase in the number of functional mitochondria within the dendrites of neurons expressing FUSR521G. f Neuron cultures co-stained with CellROX, anti-MAP2 and DAPI. g Treatment with IMS-088 blocks the production of reactive oxygen species in neurons expressing FUSR521G. Values from each group are expressed as mean ± SEM. Statistics uses a one-way ANOVA for multiple group comparisons (n = 3–4 biological replicates/group). *p < 0.05, **p < 0.01, ****p < 0.001, and not significant (ns)

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