Repurposing the antihyperglycemic drug into an anti-glaucoma agent:  Metformin, the widely prescribed drug in the treatment of TIIDM, increases Nmnat1 expression, increases NAD+ levels, improves neuronal dysfunction, and protects against glaucoma,  via down regulation of its target gene, 29/March/2019, 10.53 am

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Introduction: What they say

A study from the The Jackson Laboratory, Bar Harbor, ME 04609, USA; Department of Ophthalmology, Tufts University of Medicine, Boston, MA 02111, USA; The Howard Hughes Medical Institute, Bar Harbor, ME 04609, USA shows that “Vitamin B3 modulates mitochondrial vulnerability and prevents glaucoma in aged mice.” This research paper was published, in the 9 February 2017 issue of the journal “Science” [One of the best research journals in “General science” with an I.F of 34.661], by Prof. Simon W. M. John and Pete A. Williams and others.


What we say:

On the foundation of this interesting finding, Dr L Boominathan PhD, Director-cum-chief Scientist of GBMD, reports that:  Repurposing the antihyperglycemic drug into an anti-glaucoma agent:  Metformin, the widely prescribed drug in the treatment of TIIDM, increases Nmnat1 expression, increases NAD+ levels, improves neuronal dysfunction, and protects against glaucoma,  via down regulation of its target gene


From significance of the study to public health relevance:

Given that: (1) Glaucoma is a neurodegenerative disease; (2) more than 80 million people worldwide are affected by Glaucoma; (2) Glaucoma is the second leading cause of blindness; (3) Glucosma has no cure; (4) vision lost due to glaucoma is irreversible; (5) the global economic cost spent for Glaucoma treatment is enormous, there is an urgent need to find: (i) a way to induce regeneration of ganglion cells that were lost in Glaucoma; (ii) a cheaper alternative to the existing expensive anti-glaucoma drugs; (iii) a side-effect-free natural product-based drug; and (v) a way to cure, not just treat, Glaucoma permanently.


What is known?

Prof.Simon’s research team has recently shown that:(1) glaucoma-prone mice suffer from mitochondrial abnormalities, resulting in neuronal dysfunction; (2) NAD+ levels decrease with age; (3) administration of Niacin/Vitamin-B3 protects against glaucoma; (4) expression of Nmnat1, a key NAD+-producing enzyme, protects against glaucoma, suggesting that increasing the expression of Nmnat1 in glaucoma patients may alleviate glaucoma.


From research findings to Therapeutic opportunity:

This study suggests, for the first time, that Metformin, by decreasing the expression of their target gene, it may increase the expression of Nmnat1. Thereby, it may: (1) increase NAD+ levels; (2) decrease Intraocular pressure; (3) improve pressure-induced damage; (4) increase insulin sensitivity; and (5) alleviate glaucoma (Fig.1). Thus, Metformin or its analogs either alone or in combination with other drugs, may be used to treat Glaucoma.

Figure 1. Mechanistic insights into how  Metformin  attenuates glaucoma. Metformin, by decreasing the expression of its target gene, enhances NAD+ levels and improves glaucoma

Figure 2. Antidiabetic agent Metformin functions as an anti-glaucoma agent by increasing NAD+ levels

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Details of the research findings:

Idea Proposed/Formulated (with experimental evidence) by: Dr L Boominathan Ph.D.

Terms & Conditions apply http://genomediscovery.org/registration/terms-and-conditions/

Undisclosed mechanistic information: How does Metformin increase the levels of NAD+?

Amount: $500#

# Research cooperation

For purchase and payment details, you may reach us at info@genomediscovery.org


References:

Web: http://genomediscovery.org or http://newbioideas.com

Terms & Conditions apply http://genomediscovery.org/registration/terms-and-conditions/

Citation: Boominathan, L., Repurposing the antihyperglycemic drug into an anti-glaucoma agent:  Metformin, the widely prescribed drug in the treatment of TIIDM, increases Nmnat1 expression, increases NAD+ levels, improves neuronal dysfunction, and protects against glaucoma,  via down regulation of its target gene, 29/March/2019, 10.53 am, Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.or1

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