Stephanie C Joachim
University Eye Hospital, Ruhr-University Bochum, Germany
Title: Inflammatory demyelination induces retinal ganglion cell loss and glia response in experimental autoimmune encephalomyelitis
Biography
Biography: Stephanie C Joachim
Abstract
During multiple sclerosis (MS), inflammatory demyelinating lesions develop in the CNS. Patients can experience permanent vision loss after optic neuritis occurs. In an experimental autoimmune encephalomyelitis (EAE) model cell infiltrations (p = 0.0047) and demyelination (p = 0.0018) of EAE nerves strongly correlates with the clinical signs (r> 0.8). In the retina, EAE leads to a significant loss of retinal ganglion cells (RGCs; p< 0.0001). Additionally, an increased apoptosis rate is noted in these retinas (p = 0.0222). EAE also leads to a long lasting activation of microglia (p < 0.05) and a macroglia response in ocular tissues, probably due to the apoptosis of RGCs. Based on our findings, we propose, EAE first starts as an autoimmune disease by causing neuroinflammatory responses against the myelin sheaths. This results in demyelination and inflammation in the optic nerve. In the second phase, it continues as a neurodegenerative disease noticeable by apoptosis of RGCs due to axon demyelination. During the third phase, the apoptosis of RGCs induces to an activation of inflammatory processes in the retina, like IL-6 production and activation of astrocytes and microglia.