Corso Residenziale Siena 2011
- OPAI mutations induce mitochondrial DNA instability and optic atrophy "plus" phenotypes
- Oestrogens ameliorate mitochondrial dysfunction in Leber's hereditary optic neuropathy
- Melanopsin retinal ganglion cells are resistant to neurodegeneration in mitochondrial optic neuropathies
- Multi-system neurological disease is common in patients with OPA1 mutations
- Mitochondrial dysfunction as a cause of optic neuropathies
- OPAI mutations associated with dominant optic atrophy impair oxidative phosphorylation and mitochondrial fusion

