"The effect was strong but absent a direct head-to-head comparison it might be a bit too much to say that Dimebon blows the competition out of the water," said Karl Herrup, chair of the Cell Biology and Neuroscience Department at Rutgers University in Piscataway, N.J.
"The question would be whether it has an additive effect if it were administered along with current medicines," Herrup said. "Since it may be acting through the same pathways, there may be no added benefit."
Dr. Doody's team originally thought Dimebon worked in the same way as the two main types of Alzheimer's drugs &$151; cholinesterase inhibitors and NMDA-receptor antagonists. But now Doody suspects Dimebon might functions differently.
"This drug does both of those functions, but weakly," Doody said. "We think that those two drug actions are really not important to why it was successful."
Instead, Doody believe Dimebon's action centers around mitochondria — the so-called power plants of cells — keeping brain cells functioning, maintaining communication between brain cells and potentially protecting them from death. Yet all of that still only treats the symptoms of Alzheimer's.
"This drug and all the others are not cures for the disease," Doody said. "This is promising … but it's not marketed anywhere in the world right now, and it hasn't been approved in any country."
Doody and her team are recruiting for a six month, Phase III FDA trial in the U.S., Europe and South America. The results of that trial will determine whether Diebon moves on to the the FDA drug approval process.