Ahmara Ross
University of Pennsylvania, PA·Neuroscience
Glaucoma slowly destroys the nerve cells that connect the eye to the brain, and about half of the three million Americans with primary open-angle glaucoma (POAG) do not know they have it. Genetics raises the risk almost ninefold.
- Fields
Neuroscience
Genetics
Medicine & Clinical Research
- Topics
glaucoma
WD40 domain
retinal ganglion cells
- Grants
- 1 known grant, through Aug 2027
What they work on
- Determine how WDR36 WD40-domain variants affect retinal ganglion cell survival and shape, using a WDR36 mutant mouse and RGCs grown from human stem cells with patient mutations.
- Test whether gene augmentation, delivering normal WDR36 with viral vectors, halts or reverses retinal ganglion cell loss in mouse and human stem-cell models of WDR36-linked glaucoma.
- Examine how WDR36 variants disrupt the p53-MDM2 pathway, which controls programmed cell death, in stem-cell-derived retinal ganglion cells.
- Test whether gene augmentation or specific inhibitors of the p53-MDM2 pathway slow early retinal ganglion cell degeneration in cells carrying WDR36 mutations.
More about the research
Finding the genes involved could help predict who is at risk, catch the disease earlier, and point to treatments that address its cause. One such gene is WDR36. Variants in WDR36 appear in 5.6% of POAG patients versus 1% of people without glaucoma, and some variants are linked to severe, early-onset disease.
Why it matters
People who carry WDR36 variants in its WD40 domain could gain better glaucoma risk prediction and earlier detection. Gene augmentation therapy, or drugs acting on the p53-MDM2 pathway, could slow or prevent early loss of retinal ganglion cells in these patients. The work may also offer a framework for studying other inherited forms of primary open-angle glaucoma.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Wonkyu Ju
University of California-San Diego, CA·Neuroscience
Define how AIBP, a cholesterol-removing protein, controls activation of the inflammatory receptor TLR4 within lipid rafts of Müller glia, the retina's main support cells.
Osamah Saeedi
University of Maryland, Baltimore, MD·Medicine & Clinical Research
Confirm with transgenic mouse models that adaptive optics optical coherence tomography (AO-OCT) signals specifically report retinal ganglion cell bodies and vascular pericytes, validating the imaging against gold-standard histology.
Mihyun Nam
University of Colorado Denver/Anschutz Medical Campus, CO·Medicine & Clinical Research
Compare levels of advanced glycation end products (AGEs), sugar-damaged proteins, in trabecular meshwork tissue from primary open-angle glaucoma patients and healthy controls.
The school
University of Pennsylvania: 90 labs on PI Pages, $2.2B a year on research, 750 research doctorates a year.
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