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Abstract Title:

Vitamin B3 modulates mitochondrial vulnerability and prevents glaucoma in aged mice.

Abstract Source:

Science. 2017 Feb 17 ;355(6326):756-760. PMID: 28209901

Abstract Author(s):

Pete A Williams, Jeffrey M Harder, Nicole E Foxworth, Kelly E Cochran, Vivek M Philip, Vittorio Porciatti, Oliver Smithies, Simon W M John

Article Affiliation:

Pete A Williams

Abstract:

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 B3), and/or gene therapy (driving expression of Nmnat1, 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 B3 in glaucoma and potentially other age-related neurodegenerations.

Study Type : Animal Study

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