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Adv."],"published-print":{"date-parts":[[2026,2,20]]},"abstract":"<jats:p>\n                    Autosomal dominant optic atrophy (ADOA) is a hereditary optic neuropathy caused by\n                    <jats:italic toggle=\"yes\">OPA1<\/jats:italic>\n                    variants, leading to retinal ganglion cell (RGC) degeneration and vision loss. The mechanisms behind RGC vulnerability to mitochondrial dysfunction remain unclear. We developed a patient-specific\n                    <jats:italic toggle=\"yes\">\n                      Opa1\n                      <jats:sup>V291D\/+<\/jats:sup>\n                    <\/jats:italic>\n                    knock-in mouse model to investigate mitochondrial dysfunction and retinal metabolism in ADOA. We observed that\n                    <jats:italic toggle=\"yes\">\n                      Opa1\n                      <jats:sup>V291D\/+<\/jats:sup>\n                    <\/jats:italic>\n                    mice exhibited anatomical and functional RGC abnormalities recapitulating the ADOA phenotypes. Reduced optic atrophy 1 (OPA1) protein levels were noted in\n                    <jats:italic toggle=\"yes\">\n                      Opa1\n                      <jats:sup>V291D\/+<\/jats:sup>\n                    <\/jats:italic>\n                    mice, accompanied by decreased protein stability. Moreover, mitochondrial function was compromised, as indicated by reduced Complex I activity, increased oxidative stress, and diminished adenosine triphosphate production in the retinas of\n                    <jats:italic toggle=\"yes\">\n                      Opa1\n                      <jats:sup>V291D\/+<\/jats:sup>\n                    <\/jats:italic>\n                    mice. Spatial metabolomics revealed energy deficits in the inner retina and heightened glycolysis in the outer retina. Immunostaining showed decreased expression of glycolytic proteins in the ganglion cell layer. Single-nucleus RNA sequencing disclosed significant down-regulation of energy-production genes in RGCs, while other retinal cell types remained unaffected. These findings emphasize the specific vulnerability of RGCs to bioenergetic crises, connecting disrupted energy homeostasis to their degeneration. By increasing the nicotinamide adenine dinucleotide (NAD\n                    <jats:sup>+<\/jats:sup>\n                    )\/reduced form of NAD\n                    <jats:sup>+<\/jats:sup>\n                    (NADH) redox ratio through the overexpression of mitochondrial-targeted\n                    <jats:italic toggle=\"yes\">Lactobacillus brevis<\/jats:italic>\n                    NADH oxidase (\n                    <jats:italic toggle=\"yes\">MitoLbNOX<\/jats:italic>\n                    ) in RGCs, we demonstrated improved RGC function and survival through enhanced energy metabolism and reduced oxidative stress. These findings confirm that disrupted energy metabolism leads to RGC degeneration and emphasize the enhancement of the NAD\n                    <jats:sup>+<\/jats:sup>\n                    \/NADH redox ratio as a promising treatment strategy to protect RGCs from degeneration in ADOA.\n                  <\/jats:p>","DOI":"10.1126\/sciadv.adx7815","type":"journal-article","created":{"date-parts":[[2026,2,18]],"date-time":"2026-02-18T18:59:51Z","timestamp":1771441191000},"update-policy":"https:\/\/doi.org\/10.34133\/aaas_crossmark","source":"Crossref","is-referenced-by-count":2,"title":["Disrupted energy metabolism is associated with retinal ganglion cell degeneration in autosomal dominant optic atrophy"],"prefix":"10.1126","volume":"12","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-6814-6530","authenticated-orcid":true,"given":"Eugene Yu-Chuan","family":"Kang","sequence":"first","affiliation":[{"name":"Department of Ophthalmology, Vagelos College of Physicians and Surgeons, Columbia University Irving Medical Center, New York, NY 10032, USA."},{"name":"Department of Ophthalmology, Chang Gung Memorial Hospital, Linkou Medical Center, Taoyuan 333, Taiwan."},{"name":"Graduate Institute of Clinical Medical Sciences, College of Medicine, Chang Gung University, Taoyuan 333, Taiwan."},{"name":"School of Medicine, Chang Gung University, Taoyuan 333, Taiwan."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yun-Ju","family":"Tseng","sequence":"additional","affiliation":[{"name":"Department of Ophthalmology, Vagelos College of Physicians and Surgeons, Columbia University Irving Medical Center, New York, NY 10032, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7524-1218","authenticated-orcid":true,"given":"Wei-Hao","family":"Peng","sequence":"additional","affiliation":[{"name":"School of Medicine, National Tsing Hua University, Hsinchu 300, 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