| NEW YORK
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
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
SOURCE: The Lancet Neurology, April 30, 2008.