Alzheimer's vaccine cleared plaques but did not slow disease

Alzheimer's vaccine cleared plaques but did not slow disease

A new study by researchers in the UK found that a promising vaccine designed to protect against the amyloid protein plaques that form in the brains of people who develop Alzheimer's was effective at clearing the plaques, but it did not stop the neurodegeneration associated with the disease, leading them to question current assumptions about the role that plaques play in the progression of Alzheimer's.

The study was conducted by Dr Clive Holmes at the Memory Assessment and Research Centre at Moorgreen Hospital in Southampton, UK, and colleagues, and is published in the 19th July issue of The Lancet, which this week is dedicated to dementia research.

According to the UK's Alzheimer's Society, 1 in 6 persons over 80 has dementia, and 1 in 3 older people ends their life with a form of dementia. 700,000 people in the UK are currently living with dementia, about half of them with Alzheimer's. By 2051, there will be 1.7 million people in the UK living with dementia.

The Washington Post reports that the National Institutes of Health estimates there are 4.5 million Americans living with Alzheimer's, or 1 in 20 persons aged between 65 and 74. This figure becomes one in every 2 above the age of 85.

Holmes and colleagues looked at data from 80 Alzheimer's patients who were taking part in a trial of the experimental vaccine known as AN1792 that was designed to slow or reverse the disease by removing the protein amyloid plaques that form in the brain tissue. Animal experiments have suggested this would happen, and the animals treated with the vaccine did show signs of improved brain function after the plaques were removed.

Holmes said that a long term follow up of the patients treated with the vaccine showed not only that the plaques reduced, but virtually disappeared, reported the Washington Post.

But unfortunately the researchers found no evidence that the patients benefited from the removal of the plaques.

"Even those subjects with virtually complete removal continued to deteriorate and had severe end-stage dementia prior to their death," said Holmes in a statement reported by the Post.

It would seem that the plaques are not the only reason the disease progresses, and that removing them in this way is not going to make a significant impact on patients with established Alzheimer's. Perhaps plaques are involved in early disease development, but once that reaches a certain point, something else takes over and plaques are then just a vestige of the earlier process, albeit still increasing with disease progression.

The researchers suggest that new approaches should not focus on removal of plaques, but on preventing them building up in the first place.

Susanne Sorensen, Head of Research at UK's Alzheimer's Society, said:

"It is encouraging that this drug successfully removes these plaques, but disappointing that these initial results suggest it did not slow the progression of the disease."

"More detailed evaluations of the effects of this drug are now taking place and larger clinical trials are underway. We look forward to the outcomes to establish the effectiveness of this vaccine," she added.

"Long-term effects of A(beta)42 immunisation in Alzheimer's disease: follow-up of a randomised, placebo-controlled phase I trial."

Clive Holmes, Delphine Boche, David Wilkinson, Ghasem Yadegarfar, Vivienne Hopkins, Anthony Bayer, Roy W Jones, Roger Bullock, Seth Love, James W Neal, Elina Zotova, James A R Nicoll.

The Lancet Vol 372, Number 9634, 19 July 2008, pp 216-223.

Click here for Abstract.

Sources: Journal Abstract, Washington Post, Alzheimer's Society UK.

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Section Issues On Medicine: Disease