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Exploring leber’s hereditary optic neuropathy cause reveals a mitochondrial dysfunction disorder that impairs cellular respiration. The mutations disrupt complex I of the mitochondrial respiratory chain, reducing ATP production and increasing harmful reactive oxygen species. Over time, these biochemical changes trigger apoptosis in retinal ganglion neurons and their axons, which form the optic nerve. As more cells are lost, central vision deteriorates rapidly, typically affecting one eye first before the other. Although carriers may never develop symptoms, environmental stressors and other genetic factors may influence whether vision loss occurs.

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