Neuronal NF-κB ablation does not influence neuro-axonal degeneration in experimental autoimmune demyelination

Neuro-axonal damage is a major hallmark of multiple sclerosis (MS). To date, not much is known on the underlying mechanisms of neuronal degeneration. In disease model myelin oligodendrocyte glycoprotein induced experimental autoimmune encephalomyelitis (MOG-EAE), there is a significant loss of alpha motorneurons in the cervical as well as thoracic and lumbar spinal cord. We further investigate the role of activated NF-κB for neuronal damage in a conditional ablation mouse model. A calcium calmodulin kinase II promoter-driven tetracycline transactivator is employed to regulate the expression of a human transdominant negative IκB-alpha mutant in the basal forebrain and selected neuronal subpopulations in the cerebellum and spinal cord including cerebellar Purkinje cells and spinal cord alpha motorneurons. In these mice with conditional neuronal NF-κB ablation, the clinical course of MOG-EAE, parameters of inflammation and axonal densities in the spinal cord white and grey matter as well as numbers of alpha motorneurons are not different to littermate controls. In conclusion, neuronal NF-κB ablation does not modulate neurodegeneration in autoimmune demyelination.