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Abstract #71509 Published in IGR 18-3
Vitamin B3 modulates mitochondrial vulnerability and prevents glaucoma in aged mice
Williams PA; Harder JM; Foxworth NE; Cochran KE; Philip VM; Porciatti V; Smithies O; John SWScience 2017; 355: 756-760
See also comment(s) by Keith Martin • Louis Pasquale • Harry Quigley • Derek Welsbie • Pete Williams & Simon John •
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.
The Jackson Laboratory, Bar Harbor, ME 04609, USA.
Full articleClassification:
5.1 Rodent (Part of: 5 Experimental glaucoma; animal models)
15 Miscellaneous
3.5 Molecular biology incl. SiRNA (Part of: 3 Laboratory methods)
3.6 Cellular biology (Part of: 3 Laboratory methods)
