Optic neuritis is an acute inflammatory
demyelinating disorder of the optic nerve (ON) and is an initial symptom of
multiple sclerosis (MS).
Optic neuritis is characterized by ON degeneration and retinal ganglion cell (RGC) loss that contributes to permanent visual disability and lacks a reliable treatment. Here, we used the
experimental autoimmune encephalomyelitis (EAE) mouse model of MS, a well-established model also for
optic neuritis. In this model, C57BL6 mice, intraperitoneally injected with a fragment of the
myelin oligodendrocyte glycoprotein (MOG), were found to develop
inflammation, Müller cell
gliosis, and infiltration of macrophages with increased production of
oncomodulin (OCM), a
calcium binding protein that acts as an atypical trophic factor for neurons enabling RGC axon regeneration. Immunolabeling of
retinal whole mounts with a Brn3a antibody demonstrated drastic RGC loss. Dietary supplementation with Neuro-FAG (nFAG®), a balanced mixture of
fatty acids (FAs), counteracted inflammatory and gliotic processes in the retina. In contrast, infiltration of macrophages and their production of OCM remained at elevated levels thus eventually preserving OCM trophic activity. In addition, the diet supplement with nFAG exerted a
neuroprotective effect preventing MOG-induced RGC death. In conclusion, these data suggest that the balanced mixture of FAs may represent a useful form of diet supplementation to limit inflammatory events and death of RGCs associated to
optic neuritis. This would occur without affecting macrophage infiltration and the release of OCM thus favoring the maintenance of OCM neuroprotective role.