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Disease-modifying drug may slow Alzheimer's disease

NEW YORK (Reuters Health) - The results of a clinical trial suggest that a new drug slows the functional decline seen in patients with mild Alzheimer’s disease, according to a report in the online issue of The Lancet Neurology.

The drug is called tarenflurbil, which is an agent that selectively and safely lowers amyloid-beta-42, which form amyloid. The major characteristic of the disease is the formation of amyloid plaques in the brain, which are the target of most Alzheimer’s disease therapies.

This is “the first, or one of the first, completed phase II studies of a disease-modifying as opposed to symptom-modifying treatment” for Alzheimer’s disease, lead author Dr. Gordon K. Wilcock, from the John Radcliffe Hospital in Oxford, UK, told Reuters Health.

The study involved 210 community-dwelling patients who were randomly assigned to receive tarenflurbil, at a dose of 400 mg or 800 mg, twice per day or placebo for 12 months. In a 12-month extension phase, tarenflurbil-treated patients continued the drug at the same dose, while those initially given placebo were randomly assigned to receive the active agent at either dose.

In patients with mild Alzheimer’s disease, the 800-mg dose of tarenflurbil was significantly better than placebo in slowing the decline in activities of daily living and global function, but it did not slow the decline in cognitive ability.

With moderate Alzheimer’s disease, by contrast, tarenflurbil offered no functional benefits and actually had a negative effect on the results of one dementia test.

Patients with mild Alzheimer’s disease who received tarenflurbil 800 mg during both the initial and extension phases had significantly lower rates of decline in activities of daily living, global function, and cognition than did patients initially treated with placebo.

In light of the encouraging findings, phase III studies are now underway, Wilcock said. “We will know more about the value of an anti-amyloid approach after the phase III studies report, but it implies that disease modifying strategies may be on the horizon.”

SOURCE: The Lancet Neurology, April 30, 2008.