Saturday, May 17, 2008

Prozac might cure "lazy eye", scientists say

By Ben Hirschler Friday, Apr. 18, 2008; 4:31 AM

LONDON (Reuters) - Prozac, the popular antidepressant, might also be an effective treatment for adults with a "lazy eye", according to new research.

A team of Italian and Finnish scientists said on Thursday that the medicine helped correct the eyesight of rats whose vision had been impaired in early development and it could well do the same for humans.

The medicine appears to work by returning neurons in the adult brain to a more "plastic" state normally only seen in youth. This allows the visual perception system to develop its proper connections between the eye and the brain.

The discovery could also help explain exactly how antidepressants help regulate mood in depressed patients, by suggesting brain plasticity is a key part of the process.

Prozac was initially introduced by U.S. drugmaker Eli Lilly and Co in 1987 and belongs to a class of compounds called selective serotonin reuptake inhibitors (SSRIs). It is now off patent and widely available generically as fluoxetine.

Jose Fernando Maya Vetencourt from Scuola Normale Superiore in Pisa and colleagues intend to go on to study the drug's curative properties on human eyesight, though definitive clinical trial plans have yet to be developed.

"It will take a couple of years, maybe more," he told Reuters.

Amblyopia, commonly known as "lazy eye", is the most frequent cause of visual impairment in childhood and affects 2 to 3 percent of children, according to the U.S. National Eye Institute.

Unless it is successfully treated, it usually persists into adulthood. Treatment involves making the child use the weaker eye, either by applying an eye patch or by putting drops in the stronger eye to temporarily blur the vision.

There is no proven treatment for adults.

Vetencourt said the ability of Prozac and perhaps other SSRIs to return neurons to a more plastic state could, in theory, mean they might also have a role in other neurological disorders in which synaptic plasticity was compromised, including Alzheimer's disease.

The team's findings were published in the journal Science.


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