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Dimebon Shines as Alzheimer's Therapy

Alzheimer's Stable With Dimebon; Alzheimer's Drug Rember Looks Good, Too


"Dimebon does appear to preserve function at an improved state for quite a long time," Gandy tells WebMD. "But it is not clear this is anything more than a symptomatic drug -- and if it doesn't modify the disease, it will eventually wear off."

How does Dimebon work? Nobody knows for sure. There's evidence the drug affects mitochondria -- the power plants that energize cells -- fixing a defect that kills brain cells. That may be why the drug also seems to help patients with Huntington's disease.

"Improvements in mitochondrial health affect all cells," Hung says. "In our trial, we saw fewer adverse events in Dimebon patients than in control patients. So we are not only seeing beneficial effects, but the drug is better tolerated than placebo. That is a very attractive profile for patients."

Anti-Tangle Drug Rember

Plaque isn't the only thing that clogs the brains of people with Alzheimer's disease. There's also a buildup of fibrous tangles, made up of a protein called tau. These tangles appear in the brain before symptoms appear -- and the more tangles there are, the worse the disease gets.

TauRX Therapeutics of Singapore is developing a drug called Rember that dissolves tau tangles and prevents tau from forming new tangles.

In a 321-patient trial in the U.K. and in Singapore, patients with mild-to-moderate Alzheimer's disease were treated with Rember or placebo.

After 19 months of treatment, Rember-treated patients had no decline in cognitive function. Brain scans suggested the drug reduced tangle density in parts of the brain critical for memory, according to a conference report by Claude Wischik, chairman of TauRx Therapeutics and professor of psychiatric gerontology at the University of Aberdeen, Scotland.

"This is an unprecedented result in the treatment of Alzheimer's disease," Wischik says in a news release. "We have demonstrated for the first time that it may be possible to arrest the progression of this disease by targeting the tangles which are highly correlated with the disease."

Gandy says the development of an anti-tangle drug is "great," especially since there are dementias other than Alzheimer's in which tangles, not amyloid plaque, are the problem.

"Tau is a legitimate drug target," Gandy says. "I think it may very well be that we will one day have a cocktail of anti-amyloid and anti-tau drugs to offer patients."

A phase III clinical trial of Rember will start soon, as will a planned trial in patients with Parkinson's disease. Should the Alzheimer's trial succeed -- always a big "if" -- the manufacturer says the drug could be available by 2012.

Anti-Plaque Drug PBT2

The Australian firm Prana Biotechnology is developing the plaque-busting drug PBT2, which attacks the particularly sticky protein called beta-amyloid 42.

In a 12-week trial, the drug significantly reduced beta-amyloid-42 levels in the brains of 78 patients with mild Alzheimer's disease, although it had no effect on mental function, according to a conference report by Jeffrey L. Cummings, MD, of the David Geffen UCLA School of Medicine.

"These results indicate PBT2 is having an impact on the underlying biology of Alzheimer's, which is very exciting," Cummings says in a news release. "This is a critical proof of concept, and the safety and efficacy demonstrated by PBT2 in this study warrant evaluation in a larger-scale clinical trial."

Gandy says that although PBT2 looks promising in this phase II clinical trial, the Flurizan failure shows that success can't be guaranteed until phase III trials are completed.

But Gandy hopes that an anti-amyloid drug such as PBT2 will eventually be available, possibly to combine with an anti-tau drug such as Rember and with a drug like Dimebon that has a totally different effect.


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