Brain Images Suggest Alzheimer's Drug Could Work


Last Updated: 2010-03-01 18:30:15 -0400 (Reuters Health)

By Ben Hirschler

LONDON (Reuters) - New imaging technology suggests an experimental drug for Alzheimer's reduces clumps of plaque in the brain by approximately 25%, giving potential new life to a medicine that disappointed in clinical tests two years ago.

The drug, bapineuzumab, could be the first to treat the underlying cause of the disease.

In July 2008, however, bapineuzumab failed to meet its main goal in a mid-stage trial and caused brain swelling at higher doses. More recently, in a phase 2 trial in patients with mild to moderate Alzheimer's disease, bapineuzumab had no effect on the primary outcomes, but post hoc analyses showed some benefit in APOE epsilon4 noncarriers (see Reuters Health story of December 29, 2009),

The new imaging study, which only involved 28 patients, is another modest boost.

"It demonstrated that the drug has an effect on the pathological hallmark of Alzheimer's disease," lead researcher Dr. Juha Rinne from Finland's University of Turku told Reuters.

Dr. Rinne and colleagues used a novel imaging substance that adheres to brain regions with beta amyloid plaque.

After 78 weeks, they found that patients given bapineuzumab had about a 25% reduction in plaque compared with a placebo group. The effect was similar with three different doses of the drug, they reported online March 1st in the journal Lancet Neurology.

The treatment was generally well tolerated, although two patients on the highest dose had short-term brain swelling. The drug's developers have since dropped the top dose from large ongoing later-stage trials.

Commenting on the results, Dr. Sam Gandy from New York's Mount Sinai School of Medicine said it was too early to say effective disease-modifying drugs were at hand, but the ability to measure plaque in living subjects was "something of a breakthrough."

Several drugs now approved for the Alzheimer's disease, including Namenda (memantine) and Aricept (donepezil), treat the symptoms but don't stop disease progression.

Most agents in the research pipeline, like bapineuzumab, have focused on removing clumps of amyloid plaques, which are thought to stop brain cells from functioning properly. But a rival school blames toxic tangles caused by an abnormal build-up of another protein, tau.

Lancet Neurology 2010.

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