Journal
SCIENCE
Volume 355, Issue 6326, Pages 756-760Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.aal0092
Keywords
-
Categories
Funding
- Jackson Laboratory Fellowships
- Barbara and Joseph Cohen Foundation
- Lano Family Foundation
- [EY11721]
- [HL49277]
- Div Of Biological Infrastructure
- Direct For Biological Sciences [1262049] Funding Source: National Science Foundation
Ask authors/readers for more resources
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-3), 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 B-3 in glaucoma and potentially other age-related neurodegenerations.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available