Scientists in the USA developed a pioneering gene therapy that satisfactorily restored night vision in dogs suffering from a form of congenital night blindness. The achievement offers hope that the way was opened for the treatment of people with a similar condition, congenital stagnant night blindness.
There are five different types of this condition, which are characterized by the appearance of night blindness from birth. On the contrary, the vision during the day is slightly reduced, while the perception of colors is normal. People with this condition can not see objects when it gets dark, there is not enough artificial night lighting or they drive at night. In 2015 it was discovered that dogs suffer from a similar inherited blindness and in 2019 the “guilty” gene (LRIT3) was identified.
Researchers from the University of Pennsylvania, led by Assistant Professor Keiko Mijandera of the School of Veterinary Medicine, published the paper in the journal National Academy of Sciences of the United States (PNAS). managed for the first time through gene therapy to restore night vision in dogs born with this disease. The treatment, which is a one-off and replaces the problematic gene with a healthy one, targets a group of cells deep in the retina of the eye, something that has never happened before.
The dogs were able to find their way into a maze with very dim light and the healing effect seems to be lasting, as it has an effect for over a year on the animals.
“The results of this pilot study are very promising. In humans and dogs with congenital stagnant night blindness the severity of the disease is continuous and unchanged throughout their lives. We were able to treat these dogs aged one to three years. “This makes our findings about the adult human population promising as well, as in theory we could even intervene in adults to improve their night vision,” said Dr Miyandera.
The treatment can be improved and this is what researchers will now seek. Some dogs responded better to the gene change than others, while the healthy copy of the gene was “expressed” in only 30% of the cells deep in the retina. The ultimate goal is the first clinical trial in humans.
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