
Cavities: teeth don't just fall out if we abuse sugar
14 March, 2023Call for Strategic Action in Health 2023
20 March, 20233,5% of the population between 40 and 80 years old suffers from glaucoma. And this is a lot. To give us an idea, 111 million people will suffer from this serious neurodegenerative disease that affects the optic nerve in 2040, the leading cause of irreversible blindness in the world.
One of the main problems with glaucoma is that vision loss begins at the periphery of the visual field and is not noticed; hence its nickname “silent disease”. When we detect this loss, approximately half of the neurons have already died and we cannot recover them, as happens in Alzheimer's.
fatal pressure
Among the different types of glaucoma, open-angle glaucoma is the one that most affects the European population. It is characterized by an increase in intraocular pressure, generated when there is more fluid than necessary inside the eye. This fluid, responsible for feeding the cells inside the visual organ, must be produced and eliminated at a rate that maintains normal pressure.
If the cells responsible for generating it (ciliary body) do so above their optimal level or the evacuation encounters some impediment in the filtering process, then the pressure increases. Vision loss appears when this push is transmitted to the retina, the nervous part of the eye – located in the back area – and the cells that carry the visual message to the brain die.
How is glaucoma treated?
Treatments are aimed at stopping the progression of the disease by reducing intraocular pressure. However, today it cannot be reversed and the vision already lost can be recovered. The order of therapies to prevent progression is:
Medications in the form of drops, generally aimed at reducing the production of aqueous humor or improving the drainage of said fluid.
Laser therapies on the channel through which the fluid drains. The objective is to increase this drainage and reduce intraocular pressure when the drops have no effect.
Surgery to increase the opening of a drainage area or the filtration of aqueous humor (trabeculectomy) or to implant a drainage device. It is used when the two previous phases no longer manage to reduce intraocular pressure.
Investigations in progress
Despite more than 150 years having passed since the discovery of glaucoma, we have not been able to unravel why it occurs and how it progresses. It is true that techniques to reduce pressure have improved, but we still do not know how to protect or regenerate lost neurons.
To study any disease it is necessary to analyze what is happening and test treatments on animals before they reach humans. Thus, in 2004, our working group developed a pig model of glaucoma thanks to funding from the North American foundation The Glaucoma Foundation.
We chose this animal because its eye is very similar to the human eye. Currently, this model is being used to design devices that reduce intraocular pressure.
We also develop other systems that are simpler to apply in laboratory animals such as rats. Called the microbeads method in English, it is the most used experimental glaucoma model in the world and allows us to advance our knowledge of the mechanisms that cause the death of neurons.
The research group that I currently direct has also been a pioneer in the study of neuroprotection. That is, to quantify whether, apart from reducing intraocular pressure, the treatments protect neurons from death in glaucoma.
In addition, we have collaborated with pharmaceutical companies to develop longer-lasting and easier-to-apply treatments – especially for the elderly and children – using RNA interference technologies. This would replace the daily drops prescribed in classic therapies.
And finally, we have recently discovered the role played in glaucoma by the most abundant cells in the retina, called Müller glia, which function as pressure sensors. In a normal state, they secrete factors that protect retinal neurons, but we have shown that when intraocular pressure increases, they are altered and trigger the death of neurons that cause blindness in glaucoma. These cells appear as (G ) in the schematic.
This proposal is very novel and may impact the future of glaucoma treatments. We have just presented the results at the European Vision and Eye Research Meeting. Accepted at the most prestigious international conference in the field of vision (ARVO), they will be published very soon in a high-impact scientific journal.
Without a doubt, with more investment in research we will be able to cure glaucoma and recover the sight of those who have lost it due to it. A long and hopeful road awaits us.
Read the article on the original website, clicking on the button below this text.
Source: The Conversation. Authorship:
Elena Vecino Cordero
Professor of Cellular Biology (UPV/EHU), IdEX Prof. Univ. Bordeaux (France), Life Member Clare Hall Cambridge (UK). Director of the Ophthalmo-Experimental Biology Group (GOBE), University of the Basque Country / Euskal Herriko Unibertsitatea




