A potential cure for glaucoma, previously thought to be incurable, has been discovered by a team of UC Berkeley and University of Toronto researchers, according to a study published Monday.
The teams discovered that reintroducing lipoxins, small fats that naturally protect cells, could stop neurodegenerative diseases like glaucoma. Rodents with a disease that mimicked human glaucoma developed by UC Berkeley optometry professor and co-author John Flanagan, were cured by introducing lipoxins A4 and B4.
The study’s authors have now filed for a patent to use lipoxins A4 and B4 to treat glaucoma and other neurodegenerative diseases.
According to Karsten Gronert, chair of vision science program at UC Berkeley and author of the study, astrocytes — star shaped cells in the eye, brain and spinal cord — send out chemical signals to the optic nerve. The team identified that this signal is composed of lipoxins, which maintain normal nerve cell health.
Glaucoma, the most prevalent neurodegenerative disease, causes damage to the optic nerve and deteriorates vision, leading to blindness. According to Jeremy Sivak, associate professor of ophthalmology at the University of Toronto and author of the study, there are over 70 million glaucoma patients worldwide.
This potential cure for glaucoma could potentially be used for other neurodegenerative diseases such as Parkinson’s, Alzheimer’s and Huntington’s diseases.
The researchers found these lipoxins reversed the degeneration of nervous tissue in rodents with glaucoma. According to Sivak, reaching the human trial stage requires more understanding of how this signal works to preserve tissues on a cellular level and will take years to develop a drug that could be used.
The naturally occurring lipoxins would be reinserted into the retinal tissue of the eye, and would be the first drug to stop nerve damage seen in neurodegenerative diseases, Sivak said.
Sivak and Flanagan have studied the nervous tissue of glaucoma patients together since 2010. The collaborators discovered a natural neuroprotective signal five years ago. Flanagan brought Gronert onto the project for his expertise in identifying small particles, specifically lipids.
Flanagan’s lab developed a model that replicates human laucoma in the rodent test subjects, while Gronert’s lab worked to identify what composed the neuroprotective signal.
“We discovered that lipoxins are normally present to keep the system functioning properly and they become deficient when you get the disease,” Sivak said. “If you add them back as a drug, it’s a neuroprotective signal and neuroprotective treatment. There hasn’t been any previous evidence of this kind of molecules having that kind of neuroprotective activities. It’s unconventional because they are lipids.”
Reimplementing lipoxins as a drug could help cure other neurodegenerative diseases due to their anti inflammatory and neuroprotective effects, Gronert said. Drug companies have been studying lipoxins ability to fight inflammation in these diseases for years. Thus, Gronert said the pipeline to getting human clinical trials could be sooner than typical drug development.
Both Sivak and Gronert said they began studying the eye for its unique properties.
“I’ve always been fascinated by the eye. For most people it is their window into the world, literally. Glaucoma is a terrible, insidious disease,” Sivak said. “The cause of the degeneration has been challenging to pin down on decades of research. Any insights on how to prevent it are transformative in the field.”