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Definition of dominant optic atrophy disease (DOA) is a neuro-ophthalmologic condition characterized by bilateral degeneration of the nerve receptors, which insidiously to vision loss, typically starting in the first decade of existence. The disease affects the primary retinal ganglion cells (RGC) and their axons form the optic nerve, which transmit information to the modality of the photoreceptors to the side geniculus in the brain.EpidemiologyThe prevalence of the disease varies from 1/10000 in Denmark attributable to a founder effect, to 1/30000 in the rest of the patients usually suffer worldwide.Clinical descriptionDOA temperament to loss of vision, central visual field in addition to associated or paracentral deficits and color vision deficiencies. The severity of the disease is variable, especially, the visual acuity Locomote from normal to legal blindness. The ophthalmological examination revealed optic disc pallor and atrophy isolated fundoscopy, companion of the RGC death associated.About 15% of patients DOA harbourextraocular multi-systemic functions, including neurosensory hearing loss or less commonly chronic progressive external ophthalmoplegia, myopathy, peripheral neuropathy triune sclerosis-like illness, symptom paraplegia, whether cataracts.AetiologyTwo genes (OPA1, Opa3) encode inner mitochondrial proteins and three loci (OPA4, OPA5, OPA8) are currently known for DOA. Additional loci and genes (OPA2, and OPA6 OPA7) are responsible for the X-linked recessive or optic atrophy.Each OPA identified genes do not encode mitochondrial proteins embedded in the hidden slide and ubiquitously expressed proteins such as the concern of Leber mutations in mitochondrial fusion mutiert.OPA1, energy metabolism, the stability of apoptosis, calcium clearance and maintenance of mitochondrial genome integrity. Opa3 mutations affect only the stamp of metabolism and the control of apoptosis.DiagnosisPatients are usually diagnosed during early childhood because of bilateral, moderate, otherwise unexplained visual loss associated with receptor-disc pallor and emaciation, and typically occur as part of a family history of DOA. Optical coherence tomography also revealed non-specific depletion of the membrane fiber bed chutzpah, but a native morphology of the photoreceptor layers. Abnormal visual induced potentials and pattern ERG can also be by the dysfunction of RGCs and their Axone.Molekulare diagnosis by identifying a mutation in the gene OPA1 (75% of patients DOA) ormade within the Opa3 gene (1% of patients) are available. PrognosisVisual loss in DOA may progress during adolescence into adulthood, with a very slow subsequent chronic course in most cases. On the contrary, in DOA patients with associated extraocular features of visual loss May be done intensive event.