Contributions
Abstract: P428
Type: Poster
Abstract Category: Pathology and pathogenesis of MS - 13 Experimental models
Experimental autoimmune encephalomyelitis (EAE) to immunization with myelin oligodendrocyte glycoprotein (MOG) is a widely used disease model of multiple sclerosis (MS). Although visual evoked potentials (VEPs) allow to monitor demyelination and remyelination in the clinical setting, their pathological correlate in the chronic phase of EAE still needs to be exploited. We aimed at investigating VEPs and ON histology in MOG-EAE induced in Dark Agouti (DA) rats.
Twenty-six DA rats were immunized with MOG and VEPs and histology were performed after EAE onset (day 10-12) at day 21 (n=3), 47 (n=5), 54 (n=10) and 68 (n=8) days post injection (dpi) with quantification of demyelination percentage, axonal loss percentage and number microglial activated cells in both optic nerves. A healthy control group (n=8) was monitored over the same time points and histology was performed in 2 rats. T-test for independent samples was performed for group comparisons and Pearson's coefficient for correlation analysis. At 21 dpi, VEPs were delayed for 83% of EAE eyes, while at 47 dpi all VEPs were delayed (50%) or absent (50%), with lower frequency of absent VEPs at later time points (54 dpi: 25% absent, 45% delayed; 68 dpi: 25% absent, 75% delayed). VEPs latency was significantly correlated with demyelination (Pearson's r=0,565, p< 0,0001), axonal loss (r=0,482, p=0,0003) and activated microglia (r=0.488, p=0,0002).
VEPs latencies were best correlated with the extent of demyelination rather than axonal loss or inflammation. This finding is consistent with the view that VEPs latency can be considered as an in vivo, repeatable measure to monitor demyelination in EAE for validating new models and testing drugs acting on demyelination and remyelination.
Disclosure: The authors declare no competing financial interest
Abstract: P428
Type: Poster
Abstract Category: Pathology and pathogenesis of MS - 13 Experimental models
Experimental autoimmune encephalomyelitis (EAE) to immunization with myelin oligodendrocyte glycoprotein (MOG) is a widely used disease model of multiple sclerosis (MS). Although visual evoked potentials (VEPs) allow to monitor demyelination and remyelination in the clinical setting, their pathological correlate in the chronic phase of EAE still needs to be exploited. We aimed at investigating VEPs and ON histology in MOG-EAE induced in Dark Agouti (DA) rats.
Twenty-six DA rats were immunized with MOG and VEPs and histology were performed after EAE onset (day 10-12) at day 21 (n=3), 47 (n=5), 54 (n=10) and 68 (n=8) days post injection (dpi) with quantification of demyelination percentage, axonal loss percentage and number microglial activated cells in both optic nerves. A healthy control group (n=8) was monitored over the same time points and histology was performed in 2 rats. T-test for independent samples was performed for group comparisons and Pearson's coefficient for correlation analysis. At 21 dpi, VEPs were delayed for 83% of EAE eyes, while at 47 dpi all VEPs were delayed (50%) or absent (50%), with lower frequency of absent VEPs at later time points (54 dpi: 25% absent, 45% delayed; 68 dpi: 25% absent, 75% delayed). VEPs latency was significantly correlated with demyelination (Pearson's r=0,565, p< 0,0001), axonal loss (r=0,482, p=0,0003) and activated microglia (r=0.488, p=0,0002).
VEPs latencies were best correlated with the extent of demyelination rather than axonal loss or inflammation. This finding is consistent with the view that VEPs latency can be considered as an in vivo, repeatable measure to monitor demyelination in EAE for validating new models and testing drugs acting on demyelination and remyelination.
Disclosure: The authors declare no competing financial interest