New research reveals: Niacinamide can also regulate retinal function and effectively improve glaucoma

According to WHO statistics, the number of glaucoma patients worldwide has increased to about 90 million, and the disease has become the world's largest irreversible blindness disease.

Currently, the only clinically available therapy for glaucoma is to control intraocular pressure through surgical targeted therapy.

Recently, researchers from the Eye Hospital Affiliated to Karolinska Institutet in Sweden published in "Redox Biology" the results entitled Nicotinamide provides neuroprotection in glaucoma by protecting against mitochondrial and metabolic dysfunction.

In previous experiments, researchers found that in glaucoma mice, mitochondrial abnormalities appeared before neurodegeneration, and one of the metabolites, nicotinamide adenine dinucleotide (NAD), gradually decreased in the retina with age.

In order to further reveal and clarify whether nicotinamide has a protective effect on glaucoma-related retinal ganglion cells (RGC), the researchers induced an acute glaucoma rat model (OHT) with elevated IOP and caused optic nerve degeneration through axotomy After NAM treatment of the retinal explant model, it was found that the RGC loss and nuclear contraction caused by the original IOP increase and axotomy showed a significant dose-dependent reduction, and severe acute axonal degeneration and dendrites The morphology is also significantly protected, which also indicates that nicotinamide can confer neuroprotective effects on retinal ganglion cells in a series of conditions related to glaucoma.

Nicotinamide has neuroprotective effects on OHT model rats

Considering that NAD is very important for a wide range of metabolic processes in biology, and NAM also has the potential as an intervention and preventive treatment for human glaucoma, what impact will NAM supplement therapy have on normal RGC?

The researchers tested and analyzed the IOP levels of normal rats before and after NAM treatment, as well as the metabolites of related tissues, and found that NAM supplementation reduced the IOP of normal rats, while also making the retina, optic nerve and terminal axons (SC) 6% to 30% of the metabolites have changed.

Metabolic profile of retinal ganglion cell related tissues

Later, the researchers conducted metabolomics studies on the retina, optic nerve and terminal axons (SC) of OHT model mice, and found that high intraocular pressure caused α-ketoglutarate, creatine/creatinine in these tissues, The metabolism of homocysteine ​​and glycerophosphocholine is disrupted, and the supplementation of nicotinamide can prevent this metabolic disorder caused by high intraocular pressure, and at the same time increase the decreased NAD, NADH and NAM levels in the optic nerve.

Niacinamide can prevent metabolic disorders caused by high intraocular pressure

Nicotinamide can be rapidly metabolized into NAD by the retina, optic nerve and brain tissue

Loss of mitochondrial function, remodeling or decrease in number are common features of neurodegenerative diseases.

In short, the study found that taking nicotinamide can supplement NAD that is gradually depleted with age or IOP, protect retinal ganglion cells, and effectively prevent glaucoma in animal models.

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