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Tarenflurbil found to slow functional decline in mild Alzheimer's patients
01 May 2008

Initial clinical trials of a new drug called tarenflurbil suggest that it slows the functional decline seen in patients with mild Alzheimer's disease.

The major characteristic of Alzheimer's disease is the formation of amyloid plaques in the brain, which are the target of most therapies.

The study published in the online issue of The Lancet Neurology details how tarenflurbil selectively and safely lowers amyloid-beta-42 (42-amino-acid peptide), which form amyloid.

The Phase II clinical study involved 210 community-dwelling Alzheimer's patients who were randomly assigned to receive tarenflurbil, at a dose of 400 mg (69 patients), or 800 mg twice per day (70 patients), or placebo for 12 months (71 patients).

In the report, Dr Gordon K Wilcock, from the John Radcliffe Hospital in Oxford, writes that patients receiving the 800 mg dose of tarenflurbil showed significantly better results than placebo in slowing the decline in activities of daily living and global function in patients with mild Alzeimer's disease, but it did not slow the decline in cognitive ability.

Tarenflurbil offered no functional benefits and actually had a negative effect on the results of one dementia test with patients with moderate Alzheimer's, the reports added.

However, it was found that 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.

Dr Gordon K Wilcock told Reuters this is "the first, or one of the first, completed phase II studies of a disease-modifying as opposed to symptom-modifying treatment".

"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."

Click here to learn more about Alzheimer's diseaseADNFCR-1419-ID-18576192-ADNFCR

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