Alzheimer's Research Brings Progress, Setbacks

July 19 -- FRIDAY, July 18 (HealthDay News) -- It's one step forward, one step back in the search for treatments against Alzheimer's disease.

In one of two studies in the July 19 issue of The Lancet, an older drug called dimebon significantly improved Alzheimer's symptoms. But in a second report, a once-promising vaccine failed to prevent the progression of Alzheimer's -- even though it cleared dementia-linked amyloid plaques in the brain.

This week's issue of the journal is devoted to research into the causes and treatment of dementia, including Alzheimers disease. According to the U.S. National Institutes of Health, an estimated 4.5 million Americans have Alzheimer's disease, which is thought to affect one in 20 people between the ages of 65 and 74. The estimated rate goes up to nearly half of those aged 85 and older.

In one study, British researchers led by Dr. Clive Holmes, from the Memory Assessment and Research Centre at Moorgreen Hospital in Southampton, analyzed data on 80 Alzheimer's patients who were treated with an experimental vaccine that for now is dubbed AN1792.

The vaccine is targeted at the removal of amyloid protein plaques that clump around brain cells in increasing numbers as Alzheimer's progresses. The theory was that dementia could be slowed or reversed once the plaques were cleared, and experiments in animals have shown that removing these plaques improves brain function.

Indeed, long-term follow-up of Alzheimer's patients treated with AN1792 did show, "a reduction in the number of plaques in the brains of patients -- in some cases there was a virtually complete removal of plaques," Holmes said.

But there was a catch. "Crucially, there was no evidence that the patients benefited by the removal of plaques and even those subjects with virtually complete removal continued to deteriorate and had severe end-stage dementia prior to their death," Holmes said.

Based on these results, the researcher now believes that removing plaques -- at least by this method -- is unlikely to make a significant difference to the clinical outcome of patients with established Alzheimer's disease. "In addition, it strongly suggests that plaques are not sufficient on their own to account for disease progression," Holmes said.