ArticleMolecular neurobiology2020
Gene Therapy with Single-Subunit Yeast NADH-Ubiquinone Oxidoreductase (NDI1) Improves the Visual Function in Experimental Autoimmune Encephalomyelitis (EAE) Mice Model of Multiple Sclerosis (MS).
Article in Molecular neurobiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 19 citations in OpenAlex.
- Nicotinamide Reverses the Warburg Effect in CHO Cell Culture.Biotechnology and bioengineering · 2026Article
- Xenotopic synthetic biology: Prospective tools for delaying aging and age-related diseases.Science advances · 2025Review
- Gene therapy in Aβ-induced cell and mouse models of Alzheimer's disease through compensating defective mitochondrial complex I function.Journal of translational medicine · 2024Article
- Alternative oxidase blunts pseudohypoxia and photoreceptor degeneration due to RPE mitochondrial dysfunction.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Targeting Mitochondrial Complex I Deficiency in MPPBiological procedures online · 2024Article
- Targeting NAD Metabolism for the Therapy of Age-Related Neurodegenerative Diseases.Neuroscience bulletin · 2024Review
- Optimisation of AAV-NDI1 Significantly Enhances Its Therapeutic Value for Correcting Retinal Mitochondrial Dysfunction.Pharmaceutics · 2023Article
- AAV-mediated gene therapy improving mitochondrial function provides benefit in age-related macular degeneration models.Clinical and translational medicine · 2022Article
- Gene therapy of yeast NDI1 on mitochondrial complex I dysfunction in rotenone-induced Parkinson's disease models in vitro and vivo.Molecular medicine (Cambridge, Mass.) · 2022Article
- A review of possible therapies for multiple sclerosis.Molecular and cellular biochemistry · 2021Review
- Mitochondrial function in development and disease.Disease models & mechanisms · 2021Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Mitochondrial dysfunction mediated loss of respiration, oxidative stress, and loss of cellular homeostasis contributes to the neuronal and axonal degenerations permanent loss of function in experimental autoimmune encephalomyelitis model (EAE) of multiple sclerosis (MS). To address the mitochondrial dysfunction mediated visual loss in EAE mice, self-complementary adeno-associated virus (scAAV) containing the NADH-dehydrogenase type-2 (NDI1) complex I gene was intravitreally injected into the mice after the onset of visual defects. Visual function assessed by pattern electroretinogram (PERGs) showed progressive loss of function in EAE mice were improved significantly in NDI1 gene therapy-treated mice. Serial optical coherence tomography (OCT) revealed that progressive thinning of inner retinal layers in EAE mice was prevented upon NDI1 expression. The 45% optic nerve axonal and 33% retinal ganglion cell (RGC) loss contributed to the permanent loss of visual function in EAE mice were ameliorated by NDI1-mediated prevention of mitochondrial cristae dissolution and improved mitochondrial homeostasis. In conclusion, targeting the dysfunctional complex I using NDI1 gene can be an approach to address axonal and neuronal loss responsible for permanent disability in MS that is unaltered by current disease modifying drugs.
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