Scientists Discover How to Stop Vision Loss Before It Starts

Scientists have identified molecules that can protect the eye’s cone cells from degeneration, a major cause of vision loss. The discovery points to new drug targets—and even uncovers compounds that may be harmful.

Researchers led by Botond Roska at the Institute of Molecular and Clinical Ophthalmology Basel (IOB), along with an international team, have uncovered genetic pathways and chemical compounds that can help protect cone photoreceptors. These cells are damaged in diseases such as age-related macular degeneration, a leading cause of vision loss.

Why Cone Cells Matter for Sight

Cone photoreceptors are located in the macula and play a crucial role in everyday vision tasks like reading, recognizing faces, and seeing color. When these cells die, as they do in many inherited retinal disorders and macular degeneration, central vision begins to fade. Despite years of research, there are still no approved treatments that can stop this process. This study, led by first authors Stefan Spirig, Alvaro Herrero Navarro, and colleagues, tackles that challenge using a human-based experimental model.

Large-Scale Screening Reveals Risks and Protective Compounds

The team tested more than 2,700 compounds across 20,000 human retinal organoids. Their findings revealed both promise and caution:

• Certain classes of compounds were found to harm cone cells, raising important safety concerns.
• Several molecules were identified that help protect cones from degeneration.
• Blocking casein kinase 1 emerged as a key mechanism for preserving these cells.

To carry out the study, scientists labeled cone photoreceptors so they could track their survival over time under stress conditions designed to mimic disease. This allowed for a systematic analysis of compounds with known molecular targets.

Key Mechanism Identified for Cone Survival

The researchers observed clear trends. Two kinase inhibitors repeatedly showed strong protective effects, keeping cone cells alive over extended periods. These benefits were consistent across different stress conditions and were also confirmed in a mouse model of retinal degeneration, suggesting the findings could apply more broadly.

Open Dataset to Accelerate Vision Research

In addition to identifying protective strategies, the team has made a detailed dataset publicly available. It includes information on all tested compounds, their molecular targets, and how they affect cone survival in human tissue. This resource is expected to support the development of new treatments aimed at preserving central vision and help researchers better evaluate potential retinal toxicity.

A Step Closer to Preventing Vision Loss

By combining advances in retinal biology, organoid technology, and large-scale drug screening, this work provides a strong foundation for future therapies. It brings scientists closer to a long-standing goal in eye research: protecting the cells that make clear vision possible.

 

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How coronavirus behaves in body and why Covid-19 is difficult to treat

Viruses are strange creatures. They are not even a complete cell that school textbooks describe as the basic unit of life. Viruses are a chemical compounds made up of only a handful of molecules.

These molecules arrange themselves in different orders to form various types of shapes. In the case of the novel coronavirus, these molecules make a sparkling red ball with crowns - giving identity to the family of coronavirus.

They are very, very small in size compared to their pathogenic cousins such as bacteria and fungi. They prey on almost any living organism. Some viruses infect other pathogens and make them sick. Bacteriophage is an excellent example. It infects and kills bacteria. Bacteriophage is considered as the reason why River Ganga water remained relatively bacteria-free before humans exceeded their capacity to keep the river water clean.

Coming back to viruses, they are so simple that most scientists don't even categorise them as living beings. Remember, school textbooks called them the link between the living and the non-living.

The novel coronavirus, scientifically named as SARS-CoV-2, is a comparatively large virus. Its size is about 120 nanometres - four times that of the poliovirus, which is just 30 nanometres. But a harmless Escherichia coli bacteria - the ones present in our gut - is some 16 times the size of the novel coronavirus. An average red blood cell in our body is about 64 times larger than the novel coronavirus.

The key molecule in all viruses including coronaviruses is protein. These are genetic materials and a storehouse of a very limited set of instructions - like a specific software programme. When these viruses get a favourable environment - namely, the body fluid - they start replicating themselves. This is their reproduction. They enter a cell and eat it from inside. When they leave the cell, they are in millions and the host cell is nothing more than garbage.

This is the way they wreak havoc among species including humans and crops. They are very smart and can travel through air, water, soil, droplets and from one person to other person. Through human-to-human transmission via saliva or mucous droplets, the novel coronavirus spread to all corners of the world after emerging from Wuhan in China. It took humans for a ride, literally.

Now, let's take a look at how the novel coronavirus behaves in our body. Proteins are crucial for the functioning of any living body. They don't only build muscles but they also establish the communication network within the body system. What is required, where and when, and how an issue inside the body is to be fixed is done by these proteins -- specifically, mRNA (messenger RNA), which perform the sentry's role in the body.

It is this variety of protein that keeps SARS-CoV-2 going. Typically, a human cell uses about 20,000 different types of proteins. Viruses use much less. For example, an HIV -- one that causes AIDS -- uses only 15 proteins to do its work. The novel coronavirus deploys 33, that too with the small size of its body.

Larger pathogens such as bacteria offer extra body space for medicines like antibiotics to block them from reproducing. The bacteria can be easily identified by antibiotics-induced antibodies as they flood outside the human cells. This behaviour makes them a suitable target for antibiotics/antibodies.

However, no antibiotic drug works on viruses because these germs don't reproduce on their own. They hijack the human host cell's physiology -- the miniature biological factory -- to make their Xerox copies. They leave one cell to invade millions others. They are always hidden. It is hard for medicine shots to kill viruses without damaging the body cells these pathogens have taken hostage.

There is another problem why treating viral diseases including Covid-19 is a bigger challenge. The viruses keep evolving almost continuously, but not significantly enough to be categorised as mutation. It is like changing clothes frequently.

This behaviour of virus confuses our immune system, whose responsibility is to detect the virus and neutralise the enemy. What happens often is that by the time the body's immune system detects the virus, the damage has already been done, and infection has transmitted to other person or persons.

Many a time, when body prepares for the fight with the invading virus -- the point when fever and other symptoms start showing up, the enemy is already on its way out after demolishing the fortresses of defence.

Doctors say the symptoms of fever etcetera are sometimes actually the response of the immune system rather than the virus. This is a stage where it may be too late for a patient. This is what is being seen in Covid-19 cases. A large number of Covid-19 patients died within 48 hours of their admission in a hospital. Those who were diagnosed earlier got well faster.

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University of Hyderabad faculty comes up with a potential COVID-19 vaccine

Amid a frightening picture being painted by coronavirus concerns across the world, there's a ray of hope emerging from the University of Hyderabad (UoH). In what could be a welcome breakthrough for the country and even the world, a faculty member of the biochemistry department has developed a possible vaccine against the dreaded coronavirus infection.

A statement issued by UoH states that Dr. Seema Mishra, faculty of the Department of Biochemistry, School of Life Sciences, has designed potential vaccine candidates, called T cell epitopes, against all the structural and non-structural proteins of novel coronavirus-2 (2019-nCoV) for experimental testing.

These vaccine candidates are small coronaviral peptides, molecules which are used by cells to trigger an immune response to destroy cells harbouring these viral peptides. Using powerful immunoinformatics approaches with computational softwares, Dr Seema Mishra has designed these potential epitopes in a way that can be used to vaccinate an entire population.

Usually, vaccine discovery takes 15 years, but the powerful computational tools helped in quickly enlisting these vaccine candidates in about 10 days.

A ranked list of potential candidate vaccines, based on how effectively they will be used by human cells to stop the virus, has been generated. With no matches present in human protein pool, these coronaviral epitopes pose no cross-reactivity to human cells and hence, the immune response will be against viral proteins and not human proteins. However, these results have to be investigated experimentally in order to provide conclusive evidence.

These results have been disseminated to the scientific community using ChemRxiv preprint platform for urgent experimental assays.

Acknowledging that currently social distancing remains the best defence against nCov infections, the UoH stated that vaccination will take some time as further work is needed on the candidate epitopes.

"We are hopeful that our computational findings will provide a cost-and-time-effective framework for rapid experimental trials towards an effective nCoV vaccine," the statement said.

The University of Hyderabad clarified that although the research has been disseminated, the scientific community, in vitro studies are required to be conducted for establishing the findings conclusively.

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Seizures may be predicted in people with epilepsy

Scientists have discovered a pattern of molecules that appear in the blood before seizures, which may lead to the development of an early warning system for epilepsy patients.

Researchers have discovered molecules in the blood that are higher in people with epilepsy before a seizure happens. These molecules are fragments of transfer RNAs (tRNAs), a chemical closely related to DNA that performs an important role in building proteins within the cell.

As per researchers involved in this study, tRNAs are cut into fragments when cells are stressed. Higher levels of the fragments in the blood could reflect that brain cells are under stress in the build-up to a seizure event.

Using blood samples from people with epilepsy, the researchers found that fragment levels of three tRNAs “spike” in the blood many hours before a seizure.

“People with epilepsy often report that one of the most difficult aspects of living with the disease is never knowing when a seizure will occur,” said an investigator, and the study’s lead author.

“The results of this study are very promising. We hope that our tRNA research will be a key first step toward developing an early warning system.”

The World Health Organisation estimates that more than 50 million people worldwide have epilepsy.

“New technologies to remove the unpredictability of uncontrolled seizures for people with epilepsy are a very real possibility,” said a co-author on the paper.

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