Further analysis of these trends of the vehicle- and RTL342M-treated mice on day 63 demonstrated highly significant correlations between the clinical vs. histological data, with more damage ( p < 0.003), demyelination ( p < 0.01), and lower axon counts ( p < 0.001) with increased CDIs (Fig. 1c ), lending histological support to the improved clinical outcome observed in five of six RTL342M-treated mice.
108.3 ± 18, respectively, p < 0.01) as well as a possible trend in inhibiting further tissue damage (% damage: day 20 = 4.9 ± 2.5, day 63 vehicle = 5.1 ± 5.6, and day 63 RTL342M = 1.7 ± 2.9) and ongoing demyelination (% demyelination: day 20 = 4.3 ± 3.6, day 63 vehicle = 4.1 ± 4.7, and day 63 RTL342M = 1.8 ± 1.7) (Fig. 1b ).
Such treatment using 100-μg doses of RTL342M or DRα1-mMOG-35-55 constructs significantly reversed clinical severity and showed a clear trend for inhibiting ongoing CNS damage, demyelination, and infiltration of inflammatory cells into the CNS in male mice.