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Posted: November 25, 2008

New Drug Fails Alzheimer's Testing in Humans

Alzheimer’s researchers have been set back by the failure of an experimental drug that produced promising results in testing on mice but didn’t improve memory skills in adults with mild-to-moderate Alzheimer’s disease.

The drug, developed by Merck and known as MK-677, raised levels of a natural growth hormone by releasing insulin-like growth factor 1 (IGF-1), which was shown in mice testing to reduce levels of the dangerous beta amyloid protein that forms sticky plaques in the brain and is believed to cause Alzheimer’s disease.


In announcing that further Alzheimer’s research with MK-677 had been halted, a Merck spokesman added that studies of the compound on other medical conditions would continue.


The disappointing findings, published in the medical journal Neurology, described testing that was designed to determine whether age-related declines in levels of IGF-1 trigger the accumulation of amyloid beta in Alzheimer's sufferers. Researchers ultimately wanted to see if, by restoring IGF-1, progression of the stubborn disease could be slowed.


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


Merck researchers reached their conclusion after studying 416 people with mild-to-moderate Alzheimer's who underwent brain scans and other tests. Participants were organized into two groups, with half taking MK-677 and the other half receiving a placebo. The dosing continued for one year.


Sevigny said that while the drug boosted levels of IGF-1 by 73% after one year, if failed to prevent the disease from progressing. "This compound showed no clinical benefit in the population we studied," Sevigny said in an interview with the Reuters news agency.


He said Merck proceeded with the study largely because the drug worked in mice that had a form of Alzheimer's, but that the mouse model may not have been the best at predicting what will happen in humans with the fatal, mind-robbing disease.


"We need to have better animal models to predict the efficacy of compounds in humans," Sevigny told Reuters, adding that he believed his findings, once again, underscore the complexity of Alzheimer’s disease.

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