German researchers have discovered that genes controlling blood vessel growth in the retina of mice are “switched on” by the protein serum response factor (SRF).

 

This is a major finding, as many severe eye diseases are caused by the retina containing either too few or too many blood vessels. The results of the study therefore provide a starting point for the development of treatments for defective retinae and vitreous bodies.

 

The researchers at the University of Tübingen discovered that by eliminating this protein, they could artificially induce a certain disease profile in newborn and adult mice. Among the most interesting aspects of this research are the fact that this procedure produced different results depending on the age of the mouse and the resemblance to human diseases.

 

When the SRF was switched off in embryos or newborns, the blood vessels in the retinae were not fully developed. Their eye problems resembled vitreoretinopathy or Norrie disease. In adult mice, however, the procedure produced too many blood vessels in the retina, leading to a condition similar to that found in people with AMD.

Source: http://www.sciencedaily.com/releases/2013/04/130408133509.htm

The four gene variants linked to the development of AMD do not influence how patients respond to treatment using Lucentis and Avastin.

 

The gene variants CFH, ARMS2, HTRA1 and C3 encourage the onset of AMD. Researchers wanted to find out whether they also affected patient response to drugs used to treat the “wet” form of the disease. This would have allowed them to tailor treatment based on a patient’s genetic profile.

 

The researchers also studied the genotypes of 73% of the 1,149 participants in the Comparison of AMD Treatment Trials (CATT). Then the patients’ gene types were compared to their responses to treatment. Unfortunately, they did not find an association among the genes and the treatment responses. These results confirm those from a study conducted in 2012 by the American Academy of Ophthalmology.

 

“Our genetic research team remains hopeful that gene variants that predict patient response to AMD treatments will be identified soon,” said Dr. Stephanie Hagstrom, lead researcher in the CATT study. This would enable a significant advance in ophthalmologists’ ability to individualize treatment. 

 

Source: http://www.aao.org/newsroom/release/20130213.cfm

Research on vision loss has always focused heavily on biochemical processes. However, two Swedish researchers are now stressing the importance of biomechanical processes.

 

“We have not previously understood the mechanisms behind glaucoma and retinal detachment, but we knew that these diseases had a strong mechanical component,” explained researchers Fredrik Ghosh and Linnéa Taylor at the Lund University. “Our findings could form an initial explanation as to why we develop these diseases.”

 

The researchers used technological innovations to grow retinal tissue from pigs in a mechanical state similar to that present in the living eye. This allowed them to perform longer studies before the retina lost its structure and the cells died.

 

“This gives us new tools to understand in a more concrete manner how biomechanical factors in the central nervous system influence the health of cells when we are healthy and when we suffer from diseases,” said the researchers.

 

The results show that when the biomechanical balance is disturbed, as happens in glaucoma and retinal detachment, the normal function of the retina is lost, resulting in serious vision loss.

 

Source: http://www.sciencedaily.com/releases/2013/04/130403104102.htm

 

Essilor International recently signed a global license agreement with High Performance Optics (HPO), a U.S. company that develops technology to protect the retina from blue light.

 

Until now, the two companies have been working independently to develop lenses that can filter blue light, which is emitted in large quantities from devices such as computer screens, mobile phones, digital tablets, and LED televisions. The partnership should allow for the exploitation and adoption of the technology around the world and speed its availability to the global population. The agreement does not, however, extend to Crizal Prevencia, a lens that filters blue light, which Essilor intends to launch later in the year.

 

Very pleased with the new partnership, HPO president Mike Packard stressed the importance of this type of lens in preventing diseases like AMD. “While there are multiple factors that contribute to AMD, reducing the chances of others suffering from AMD and / or the severity of this disease has been a key goal of HPO’s for many years,” he explained. “This is most gratifying to me personally.”

Sources: http://www.prnewswire.com/news-releases/high-performance-optics-licenses-essilor-201247771.html

http://www.visionmonday.com/ViewContent/tabid/211/content_id/40087/catId/103/Default.aspx

Drugs prescribed to lower cholesterol may be effective against macular degeneration.

 

Researchers at Washington University in St. Louis have found that patients with AMD and those with atherosclerosis share an inability to get rid of fat and cholesterol. In patients with the “dry” form of AMD, lipid deposits accumulate behind the retina. As they grow and multiply, they begin to destroy the central part of the eye, interfering with vision.

 

As we age, our macrophages, the immune cells that destroy cholesterol and fat, begin to malfunction. They can even become bloated with cholesterol, causing inflammation, which triggers vascularization. Those vessels characterize the “wet” form of AMD.

 

The researchers treated the macrophages of mice with a substance that helped restore levels of ABCA1, a protein that macrophages need to do their job. The macular degeneration process was reversed.

 

“Some of the therapies already being used to treat atherosclerosis target this same pathway, so we may be able to modify drugs that already are available and use them to deliver treatment to the eye,” says lead researcher Rajendra S. Apte.

Source: http://www.sciencedaily.com/releases/2013/04/130402124648.htm