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Researchers Find Way to Combat Disease-Causing Parasites

According to the World Health Organization, diseases caused by parasites afflict up to one third of the world's population and severely sicken an estimated 300 million people every year. There are treatments for parasitic diseases, but they are far from perfect. Now, researchers have discovered a new way to attack the parasites on a molecular level.

Scientists at the University of Texas Southwestern Medical Center in Dallas discovered that, much the same way hormones are responsible for sexual maturity in humans, a hormonal process leads to the maturity and reproduction of worms.

Researchers identified the hormone-like molecule, called a ligand, in the pinhead-sized worm, C elegans, which lives in the dirt, making it similar to parasites that cause disease in two billion people around the globe.

They found that when the hormonal ligand binds with a nuclear receptor inside the cell, called DAF-12, the process triggers the activation of growth genes in the worm.

When researchers blocked the process by engineering mutant worms, the parasites went into a resting state that halted their growth and sexual maturation, according to David Mangelsdorf, the study's lead author.

"In humans, the idea would be to keep it from going into its reproductive cycle. And that would eventually cause the worm to die out," he says.

Mangelsdorf notes there are drugs known as anthelmintics available to treat worm infections. But he says the drugs have some toxicity, and often have to be given repeatedly.

Mangelsdorf says that raises concerns about the drugs losing their effectiveness.

"That's unlikely to occur in this hormone receptor pathway because you are mediating a physical pathway that is native to the worm. You're not targeting a different pharmacologic pathway," he explains.

Mangelsdorf says he expects the latest research will result in new anti-parasitic drugs in not so distant future.

The study on the discovery of the worm hormone is published in the journal Cell.