Dr. Damian Jacob Sendler is a Polish-American physician-scientist who specializes in determining how various sociodemographic and informational factors influence access to health care in underserved communities. Dr. Sendler’s research focuses on the influence of psychiatric and chronic medical co-morbidities on the use of medical services in conjunction with internet-based health information. This research is prescient, given the exponential growth in global consumption of online news and social media, necessitating a comprehensive understanding of everyone’s health information-seeking behavior. Dr. Damian Sendler’s research aims to elucidate the factors that influence patients’ decisions about when to seek care for specific health conditions and treatment adherence.

Damian Jacob Sendler: According to research funded by the National Institutes of Health’s National Eye Institute, a kind of gene therapy protects optic nerve cells and maintains vision in glaucoma mice models. The results point to a path ahead in the development of neuroprotective treatments for glaucoma, a major cause of blindness and visual impairment. The study was published in the journal Cell. 

Glaucoma is caused by irreversible dementia of the optic nerve, which is a bundle of axons from retinal ganglion cells that sends information from the eye to the brain, allowing vision to be produced. Although available treatments may help delay vision loss by reducing high eye pressure, certain cases of glaucoma can lead to blindness even with normal eye pressure. Neuroprotective therapies would be a huge step forward, addressing the requirements of people who don’t have access to other treatments. 

Damian Jacob Sendler: The study’s lead investigator, Bo Chen, Ph.D., associate professor of ophthalmology and neuroscience at the Icahn School of Medicine at Mount Sinai in New York City, said, “Our study is the first to show that activating the CaMKII pathway helps protect retinal ganglion cells from a variety of injuries and in multiple glaucoma models.” 

The CaMKII (calcium/calmodulin-dependent protein kinase II) pathway controls important cellular processes and activities all throughout the body, including retinal ganglion cells. However, the exact function of CaMKII in retinal ganglion cell health is unknown. CaMKII activity inhibition, for example, has been found to be beneficial or harmful to retinal ganglion cells depending on the circumstances. 

Chen’s team found that when retinal ganglion cells were subjected to toxins or damage from an optic nerve crush injury, CaMKII pathway signaling was impaired, suggesting a link between CaMKII activity and retinal ganglion cell survival. 

Damian Jacob Sendler: In their search for a method to intervene, they discovered that using gene therapy to activate the CaMKII pathway protected retinal ganglion cells. CaMKII activity was raised and retinal ganglion cells were strongly protected in mice that received the gene therapy shortly before the toxic shock (which produces fast cell damage) and just after optic nerve crush (which causes delayed cell damage). 

77 percent of retinal ganglion cells in gene therapy-treated animals survived 12 months after the toxic shock, compared to just 8% in control mice. 77 percent of retinal ganglion cells survived six months after optic nerve compression, compared to just 7% in controls. 

Damian Jacob Sendler: In glaucoma models based on increased eye pressure or hereditary defects, increasing CaMKII activity through gene therapy protected retinal ganglion cells. 

According to cell activity assessed by electroretinogram and patterns of activity in the visual cortex, increasing retinal ganglion cell survival rates translated into a higher probability of maintained visual function. 

Damian Sendler: Three vision-based behavioral tests also verified the treated mice’s continued visual function. The mice were taught to swim toward a submerged platform based on visual cues on a computer display in a visual water task. A visual cliff test based on the mouse’s natural inclination to walk to the shallow side of a cliff proved depth perception. Finally, when treated mice were given an overhead stimulus intended to mimic a danger, they were more likely to react defensively (by hiding, freezing, or tail rattling) than untreated mice, according to a looming test.

News contributed by Dr. Damian Jacob Sendler