This might help to explain why?
AbstractPurpose: Heterozygous optic atrophy type1 (OPA1) mutations are responsible for dominant optic atrophy, and the down regulation of OPA1 expression in patients with Leber hereditary optic neuropathy may imply that Opa1 protein levels in mitochondria play a role in other spontaneous optic neuropathies as well. Mitochondrial and metabolic abnormalities may put the optic nerve at risk in primary open angle glaucoma (POAG), and this preliminary study was designed to investigate whether altered OPA1 expression might be present in the progressive optic neuropathy of POAG
If it’s already safe in ADOA they can just go straight to phase II for Glaucoma. Must be some other conditions that also have deficits in OPA1?
This might help to explain why? AbstractPurpose: Heterozygous...
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