Glaucoma, three molecules to support the energy of vision neurons

Glaucoma is today the leading cause of irreversible blindness in the world and in Italia it affects about 2.5-3% of the population, with a prevalence that increases with age. Despite therapeutic advances, it remains a complex and often silent disease in its early stages: it is estimated that about half of those affected are unaware that they have it.

The main risk factor is high intraocular pressure, and it is also the only factor on which therapy can effectively intervene. However, in recent years, research has made it clear that disease progression does not depend solely on eye pressure. In fact, many patients continue to show worsening optic nerve damage even when intraocular pressure is well controlled. This finding has contributed to changing our understanding of glaucoma, which is now increasingly considered a neurodegenerative disease, with features reminiscent of other nervous system disorders such as Alzheimer's and Parkinson's.

At the heart of this process is the progressive loss of the retinal ganglion cells, the neurons that transmit the visual information gathered by the eye to the brain. These cells have a very high energy requirement and are particularly dependent on the efficiency of the mitochondria, the organelles responsible for energy production within the cell. When mitochondrial function is impaired, neurons become more vulnerable to metabolic and inflammatory stresses, contributing to optic nerve degeneration. Against this backdrop, there is growing interest in therapeutic strategies capable not only of reducing eye pressure, but also of directly protecting vision neurons. One of the most promising lines of research concerns the support of cellular energy function through molecules that can improve the activity of mitochondria.

In recent years, several preclinical studies published in leading scientific journals have shown that certain substances involved in energy metabolism can increase the resistance of ganglion cells to glaucoma-induced stress. Among these, particular attention has been paid to nicotinamide, pyruvate and coenzyme Q10. These molecules play key roles in the bioenergetic processes of the cell. Indeed, recent research data suggest that the combination of nicotinamide, pyruvate and coenzyme Q10 is able to reduce cell death and neuroinflammation processes, while increasing the energy activity of the mitochondria. These results strengthen the hypothesis of a metabolic neuroprotection strategy in glaucoma. In other words, alongside the reduction of intraocular pressure, the aim becomes to support the vitality of nerve cells by making them more resistant to the stresses that characterise the disease. It is important to emphasise that these approaches do not replace established therapies for controlling eye pressure, which remain the mainstay of treatment. However, the possibility of flanking interventions aimed at improving cell metabolism when eye pressure is well controlled opens up interesting perspectives in the long-term management of the disease.

Research in this area is still evolving and methodologically robust clinical studies will be needed to precisely define the role of these strategies in medical practice. However, the increasing focus on the bioenergetic mechanisms of disease represents a significant shift in perspective. Understanding and supporting the metabolism of vision neurons could, in fact, become one of the key tools for slowing the progression of glaucoma and preserving patients' visual function for longer. In a disease that often remains asymptomatic for years, and which in several cases can unfortunately be diagnosed when the damage is already advanced, each step forward in protecting the optic nerve is an important contribution to protecting visual health.