The Jensen Lab is behind a single unmarked door in the basement of Morrill Science Center III.
In this lab, there are more than 6,000 of one of science’s most valuable models for studying human genetics and disease—the zebrafish. The tiny, striped members of the minnow family dart about in 200 small tanks on racks that are four rows deep.
In one particular tank, all of the zebrafish have lost their zebra; their typical five uniform, pigmented, horizontal stripes are gone. Called “crystals,” these creatures are a translucent pink, and you can see outlines of their backbones and the shadows of their tiny internal organs.
Light is actually a toxic insult upon life at the cellular level, especially on cells called photoreceptors that process light in the eye. “Their eyeballs are completely clear,” she explains. She hopes the light will degenerate, or damage, the cells. “It seems weird that we are trying to get the cells to die,” says Jensen. “But we need a model to get the cells to die so that we can understand why they die and then how to keep them alive.” Learning why the cells degenerate will improve our understanding of an eye disease that affects about one out of every 8–10 thousand young Americans: Stargardt disease.
Named for Karl Stargardt—the German ophthalmologist who first described the inherited eye disorder in 1909—Stargardt disease is a disorder of the retina that causes vision loss (though generally not complete blindness) during childhood or adolescence, though in some cases it doesn’t occur until adulthood. Vision loss progresses slowly over time in most people with the disease, from normal vision to legally blind. Currently, there is no treatment to delay or cure the disease.
Thanks to a grant from the Manning Innovation Program —a recent $40,000 gift to UMass for the support of translational research projects and the transfer of breakthroughs to the marketplace—Jensen hopes she is all the closer to finding a key that will unlock some of the secrets of Stargardt disease.
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Department of Biology