MT-ND4 and Leber hereditary optic neuropathy: Fibroblasts derived from three male patients (aged 33, 36 and 40 years) carrying the G11778A mutation in ND4 known to cause complex I dysfunction and LHON were treated with AAV-ophNdi1 to determine if the beneficial effects seen in the rotenone-induced mouse model would lead to the phenotypic rescue in these patient-derived cells, representing a model of complex I deficiency.