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UPDATE 1-Merck drug fails to slow Alzheimer's symptoms

Mon Nov 17, 2008 4:23pm EST

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(Adds status of drug, paragraph 3)

By Julie Steenhuysen

CHICAGO, Nov 17 (Reuters) - An experimental Merck & Co Inc (MRK.N) drug that raises levels of a natural growth hormone failed to improve memory skills in people with mild to moderate Alzheimer's disease, U.S. researchers said on Monday.

The compound, called MK-677, stimulates the release of insulin-like growth factor 1, or IGF-1, which has been shown in mice to reduce levels of beta amyloid protein that forms sticky plaques in the brain.

Merck spokesman Ian McConnell said the company has discontinued research on the drug in Alzheimer's disease, but studies in other conditions are still under way.

These plaques are a hallmark of Alzheimer's disease, a progressive disease marked by memory loss, confusion and eventually, the inability to care for oneself.

The study, published in the journal Neurology, was designed to test whether age-related declines in levels of IGF-1 drive the accumulation of amyloid beta in Alzheimer's patients, and if restoring IGF-1 might help slow progression of the disease.

"This work suggests that targeting this hormone system may not be an effective approach to slowing the rate of Alzheimer's disease progression," said study leader Dr. Jeff Sevigny of Merck Research Laboratories in North Wales, Pennsylvania, in a statement.

The researchers studied 416 people with mild-to-moderate Alzheimer's disease who underwent brain scans and other tests. Half of the group took MK-677 and the other half took a placebo for one year.

While the drug succeeded in boosting levels of IGF-1 by 73 percent after a year, if failed to keep the disease from advancing. "This compound showed no clinical benefit in the population we studied," Sevigny said in a telephone interview.

Sevigny said Merck proceeded with the study in large part because the drug worked in mice with a form of Alzheimer's disease, but the mouse model may not be the best at predicting what will happen in humans with Alzheimer's disease.

"We need to have better animal models to predict the efficacy of compounds in humans," he said.

There is no cure for Alzheimer's, and current drugs merely delay symptoms. Sevigny said the findings underscore the complexity of the disease.

Alzheimer's is the most common form of dementia, affecting an estimated 5.2 million people in the United States and 26 million globally, according to the Alzheimer's Association. (Editing by Will Dunham and Eric Walsh)



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