Neuroprotection mediated by ST266 requires full complement of proteins secreted by amnion-derived multipotent progenitor cells.

However, even in this cohort of mice with only mild EAE disease, an overall trend toward loss of RGCs in EAE mice was observed, and analysis of RGC survival by retinal region (central, mid-peripheral, and peripheral) showed a small but significant loss of RGCs induced by EAE in the mid-periphery ( Fig 3 ).

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The lower molecular weight ST266 fraction significantly improved optic nerve demyelination, but only showed a trend towards improved retinal ganglion cell survival.

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