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Data from Jackson Laboratory Advance Knowledge in Glaucoma (Glaucoma as a Metabolic Optic Neuropathy: Making the Case for Nicotinamide Treatment in...

Genomics & Genetics Weekly

09-14-17

Data from Jackson Laboratory Advance Knowledge in Glaucoma (Glaucoma as a Metabolic Optic Neuropathy: Making the Case for Nicotinamide Treatment in Glaucoma)

By a News Reporter-Staff News Editor at Genomics & Genetics Weekly -- Fresh data on Eye Diseases and Conditions - Glaucoma are presented in a new report. According to news reporting from Bar Harbor, Maine, by NewsRx journalists, research stated, "Mitochondrial dysfunction may be an important, if not essential, component of human glaucoma. Using transcriptomics followed by molecular and neurobiological techniques, we have recently demonstrated that mitochondrial dysfunction within retinal ganglion cells is an early feature in the DBA/2J mouse model of inherited glaucoma."

The news correspondents obtained a quote from the research from Jackson Laboratory, "Guided by these findings, we discovered that the retinal level of nicotinamide adenine dinucleotide (NAD, a key molecule for mitochondrial health) declines in an age-dependent manner. We hypothesized that this decline in NAD renders retinal ganglion cells susceptible to damage during periods of elevated intraocular pressure. To replete NAD levels in this glaucoma, we administered nicotinamide (the amide of vitamin B3). At the lowest dose tested, nicotinamide robustly protected from glaucoma (~70% of eyes had no detectable glaucomatous neurodegeneration). At this dose, nicotinamide had no influence on intraocular pressure and so its affect was neuroprotective. At the highest dose tested, 93% of eyes had no detectable glaucoma. This represents a ~10-fold decrease in the risk of developing glaucoma. At this dose, intraocular pressure still became elevated but there was a reduction in the degree of elevation showing an additional benefit. Thus, nicotinamide is unexpectedly potent at preventing this glaucoma and is an attractive option for glaucoma therapeutics. Our findings demonstrate the promise for both preventing and treating glaucoma via interventions that bolster metabolism during increasing age and during periods of elevated intraocular pressure. Nicotinamide prevents age-related declines in NAD (a decline that occurs in different genetic contexts and species). NAD precursors are reported to protect from a variety of neurodegenerative conditions. Thus, nicotinamide may provide a much needed neuroprotective treatment against human glaucoma."

According to the news reporters, the research concluded: "This manuscript summarizes human data implicating mitochondria in glaucoma, and argues for studies to further assess the safety and efficacy of nicotinamide in human glaucoma care."

For more information on this research see: Glaucoma as a Metabolic Optic Neuropathy: Making the Case for Nicotinamide Treatment in Glaucoma. Journal of Glaucoma, 2017;():. (Lippincott Williams and Wilkins - www.lww.com; Journal of Glaucoma - journals.lww.com/glaucomajournal/pages/default.aspx)

Our news journalists report that additional information may be obtained by contacting P.A. Williams, *The Howard Hughes Medical Institute, The Jackson Laboratory, Bar Harbor, ME USA. Dept. of Ophthalmology, Tufts University of Medicine, Boston, MA, United States. Additional authors for this research include J.M. Harder and S.WM John (see also Eye Diseases and Conditions - Glaucoma).

Keywords for this news article include: Maine, Genetics, Glaucoma, Bar Harbor, Neuropathy, United States, Risk and Prevention, North and Central America, Eye Diseases and Conditions, Optic Nerve Diseases and Conditions.

Our reports deliver fact-based news of research and discoveries from around the world. Copyright 2017, NewsRx LLC

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