Glaucomas are neurodegenerative diseases that cause vision loss, especially in the elderly. The mechanisms initiating glaucoma and driving neuronal vulnerability during normal aging are unknown. Studying glaucoma-prone mice, we show that mitochondrial abnormalities are an early driver of neuronal dysfunction, occurring before detectable degeneration. Retinal levels of nicotinamide adenine dinucleotide (NAD, a key molecule in energy and redox metabolism) decrease with age and render aging neurons vulnerable to disease-related insults. Oral administration of the NAD precursor nicotinamide (vitamin B), and/or gene therapy (driving expression of , a key NAD-producing enzyme), was protective both prophylactically and as an intervention. At the highest dose tested, 93% of eyes did not develop glaucoma. This supports therapeutic use of vitamin B in glaucoma and potentially other age-related neurodegenerations.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5408298 | PMC |
| http://dx.doi.org/10.1126/science.aal0092 | DOI Listing |
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