Demyelination caused by inflammation of the CNS has been considered to be a
major hallmark of multiple sclerosis (MS). Using experimental autoimmune e
ncephalomyelitis, a model of MS, we demonstrate that an immune-mediated att
ack of the optic nerve is accompanied by an early degeneration of retinal g
anglion cells (RGCs). The decrease of neuronal cell density was correlated
with functional disabilities as assessed by visual evoked cortical potentia
ls and electroretinogram. Visual acuity was significantly reduced. DNA degr
adation and activation of caspase-3 in RGCs indicate that cell death of RGC
s is apoptotic. These findings show for the first time that an inflammatory
attack against myelin components can lead to acute neuronal cell loss by a
poptosis.