All Lee Goldstein wanted to do was finish his postdoctoral research
project at a Harvard laboratory so he could get on with his career in
psychiatry. But while placing a sensor in the skull of a lab mouse, he
noticed something odd: The rodent’s eyes were milky and clouded. The
mouse had been bred to show the symptoms of Alzheimer’s disease, but
was too young to have age-related cataracts.
That was more than four years ago. Goldstein has since become a
faculty member at Harvard Medical School (and also a practicing
physician at Brigham & Women’s Hospital) and has turned that
observation of the mouse’s eyes into a potential new front in the war
against the ravages of Alzheimer’s. What he saw in the mouse, and later
found in the eyes of people who had died from the disease, were amyloid
plaques that form around the rim of the lens of the eye — long before
the same plaques in a patient’s brain start to cause the symptoms of
Alzheimer’s.
Although Goldstein’s discovery is still a long way from a diagnostic
product, its potential for catching Alzheimer’s very early is enormous.
"The most intensive area of Alzheimer’s research right now is to
determine how to slow the progression of it years or even decades
before the plaques start to cause symptoms," says Sam Gandy, the
director of the Farber Institute for Neurosciences at Thomas Jefferson
University in Philadelphia and an adviser to the Alzheimer’s
Association. "There are at least 35 drugs in development to do that
right now."
Sam Jaffe
