Drugs/Therapy

Melatonin May Help Delay Symptoms of Lou Gehrig's Disease

By Christine Hsu | Update Date: Apr 25, 2013 10:09 AM EDT

A new study revealed that melatonin, a naturally occurring hormone that plays a significant role in sleep regulation, may help delay symptoms of amyotrophic lateral sclerosis (ALS), or Lou Gehrig's disease.

Researchers found that melatonin injections delayed symptom onset and reduced mortality in mice with the neurodegenerative condition.

The latest study published in the journal Neurobiology of Disease could pave the way to the development of new ALS therapies.

Around 5,000 people are diagnosed with ALS every year.  The disease is characterized by rapidly progressive muscle weakness and eventual death due to the failure or respiratory muscles.

Researchers have been unable to find a cure or even effective treatments for ALS because the exact causes of the condition are not well understood.

After screening more than a thousand FDA-approved drugs, study authors found that melatonin is a powerful antioxidant that blocks the release of enzymes that activate apoptosis, or programmed cell death.

"Our experiments show for the first time that a lack of melatonin and melatonin receptor 1, or MT1, is associated with the progression of ALS," senior investigator Dr. Robert Friedlander, from the Pitt School of Medicine, said in a news release.

"We saw similar results in a Huntington's disease model in an earlier project, suggesting similar biochemical pathways are disrupted in these challenging neurologic diseases," he added.

Researchers treated mice bred to have an ALS-like disease treated with either melatonin or placebo injections.  They found that mice given melatonin injections developed symptoms later, survived longer, and had less degeneration of motor neurons in the spinal cord than mice in the placebo group.

"Much more work has to be done to unravel these mechanisms before human trials of melatonin or a drug akin to it can be conducted to determine its usefulness as an ALS treatment," Friedlander said.

"I suspect that a combination of agents that act on these pathways will be needed to make headway with this devastating disease," he concluded.

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