Yunshuo Tang
Washington University in St Louis, MO·Neuroscience·Early-career
Some children carry a genetic condition that predisposes them to tumors, and when a tumor grows along the nerve pathway from the eye to the brain, they can lose vision. The damage comes not from the tumor crushing the nerve but from the death of retinal ganglion cells, the neurons whose long fibers carry visual signals out of the eye.
- Fields
Neuroscience
Medicine & Clinical Research
Biology
- Topics
neurofibromatosis type 1
optic pathway glioma
low-grade astrocytoma
- Grants
- 1 known grant, through Jun 2029
What they work on
- Define whether estrogen-induced production of interleukin 1 beta, an inflammatory signal made by glial support cells, is required for retinal ganglion cell death in authenticated mouse models of Nf1 optic pathway glioma.
- Determine whether inhibiting protein kinase A, the enzyme activated by cyclic AMP, heightens the vulnerability of Nf1-mutant retinal ganglion cells, testing PKIα as a mediator of this intrinsic fragility.
- Evaluate estrogen suppression and restoration of cyclic AMP signaling as neuroprotective strategies in preclinical studies using Nf1 optic glioma mice.
- Test whether sexually dimorphic mechanisms explain why female mice and girls with Nf1 optic pathway glioma experience more vision loss, by linking estrogen signaling to retinal ganglion cell survival.
More about the research
In neurofibromatosis type 1, fifteen to twenty percent of children develop such an optic pathway glioma, a slow-growing tumor of support cells in the visual pathway, and thirty to fifty percent of them lose vision. Strikingly, girls with these tumors are three to five times more likely to need treatment for vision loss than boys, even though tumors occur about equally in both sexes. That difference suggests sex-related biology drives the neuron death, and this project aims to identify it well enough to protect vision.
Why it matters
Children with neurofibromatosis type 1 who develop optic pathway gliomas can lose sight permanently, and current tumor-directed treatment does not reliably protect the retinal neurons responsible. Pinpointing estrogen-driven inflammatory signaling and weakened cyclic AMP survival signaling as the causes of that neuron death could identify drug targets, and testing estrogen suppression and cyclic AMP restoration in mice may point toward vision-preserving therapies and help explain why girls are affected more severely.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
David H Gutmann
Washington University in St Louis, MO·Neuroscience
Define the cellular and molecular interdependencies, among tumor cells, neurons, T cells and microglia, that drive NF1-associated low-grade glioma and neurodevelopmental deficits, using patient and CRISPR-engineered iPSCs and Nf1 mutant mice.
Wendy Liu
Stanford University, CA·Neuroscience·Early-career
Determine which ultrasound parameters effectively stimulate retinal ganglion cells in the living eye, using a transparent ultrasound transducer together with two-photon calcium imaging of genetically encoded calcium indicators in animal models.
Karsten Gronert
University of California-Berkeley, CA·Neuroscience
Define which retinal cells make and respond to prostaglandin D2 (PGD2), a fat-derived signaling molecule, in healthy retina and how raised eye pressure (ocular hypertension) shuts this pathway down.
The school
Washington University in St Louis: 97 labs on PI Pages, $1.2B a year on research, 365 research doctorates a year.
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