Niacinamide can also regulate retinal function and effectively improve glaucoma

Glaucoma has become the world's largest irreversible blindness disease

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.

The optic nerve connecting the eyes and the brain of the patient will gradually be damaged, and finally blindness, age, genetic inheritance and increased intraocular pressure (IOP) have been found to be the main causes of the disease.

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

However, there is still no effective treatment for glaucoma patients with neuronal degeneration, which makes some patients still have a higher risk of blindness even after receiving treatment.

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.

The somatic cells, axons and dendritic nerves of retinal ganglion cells have a protective effect and can prevent extensive metabolic damage caused by glaucoma caused by high intraocular pressure in animal models.

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

, Which makes the retinal ganglion cells more susceptible to the pressure of IOP and accelerates the degeneration of glaucoma nerves.

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.

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.

Nicotinate and niacinamide metabolism of the entire retina and optic nerve are affected, but the effect is limited.

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.

Higher NAD has obvious axon protection, which also indicates that NAM may have a longer-term protective effect on the optic nerve.

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

After further research, the researchers found that NAM supplementation can also increase the volume and surface area of ​​mitochondria, as well as the rate and speed of migration, by increasing oxidative phosphorylation.

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.

These data help support the clinical application of nicotinamide and initiate clinical trials to determine the effect of nicotinamide on the progression of long-term glaucoma disease.

Reference materials:

[1]https:// Glaucoma has become the world's largest irreversible blindness disease

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.
The optic nerve connecting the eyes and the brain of the patient will gradually be damaged, and finally blindness, age, genetic inheritance and increased intraocular pressure (IOP) have been found to be the main causes of the disease.

Currently, the only clinically available therapy for glaucoma is to control intraocular pressure through surgical targeted therapy.
However, there is still no effective treatment for glaucoma patients with neuronal degeneration, which makes some patients still have a higher risk of blindness even after receiving treatment.
Therefore, with the intensification of population aging, the development of multi-strategy treatments for glaucoma is particularly urgent.

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.
The somatic cells, axons and dendritic nerves of retinal ganglion cells have a protective effect and can prevent extensive metabolic damage caused by glaucoma caused by high intraocular pressure in animal models.
These data also support the utility of nicotinamide as a neuroprotective therapy for human glaucoma.

In previous experiments, researchers found that in glaucoma mice, mitochondrial abnormalities occur before neurodegeneration, and one of the metabolites, nicotinamide adenine dinucleotide (NAD), gradually decreases in the retina with age.
, Which makes the retinal ganglion cells more susceptible to the pressure of IOP and accelerates the degeneration of glaucoma nerves.
Supplementing nicotinamide (NAM, vitamin B3 amide, precursor of NAD) through diet can increase NAD levels and improve the visual function of existing glaucoma patients.

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.

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.
Nicotinate and niacinamide metabolism of the entire retina and optic nerve are affected, but the effect is limited.

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.
Higher NAD has obvious axon protection, which also indicates that NAM may have a longer-term protective effect on the optic nerve.

Loss of mitochondrial function, remodeling or decrease in number are common features of neurodegenerative diseases.
After further research, the researchers found that NAM supplementation can also increase the volume and surface area of ​​mitochondria, as well as the rate and speed of migration, by increasing oxidative phosphorylation.
In turn, it provides a powerful neuroprotective effect against mitochondrial stress.

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.
These data help support the clinical application of nicotinamide and initiate clinical trials to determine the effect of nicotinamide on the progression of long-term glaucoma disease.
(Biological Exploration)

Reference materials:

[1]https://