Is the new Alzheimer's 'wonder drug' really such a miracle? - Daily Mail

As far as holy grails in medicine are concerned, you don’t get one much more significant than a cure for dementia.

And the only drugs currently available simply tackle specific symptoms of mild to moderate dementia — there is nothing that can slow down the disease or prevent it.

As far as holy grails in medicine are concerned, you don’t get one much more significant than a cure for dementia.

The drug, aducanumab (brand name, Aduhelm), works by clearing the brain of plaque, formed of a build-up of a sticky protein called amyloid-beta — this has been linked to dying nerve cells and is considered a hallmark feature of Alzheimer’s.

‘There was great hope for the amyloid-lowering drugs but the results from trials have been very disappointing,’ says Gill Livingston, a professor of psychiatry of older people at University College London.

The problem is that we still don’t understand what causes Alzheimer’s.

Based on this logic, the solution seems straightforward: clear the plaque to cure Alzheimer’s.

‘But aducanumab isn’t the transformative drug for Alzheimer’s as it generally had a small effect,’ says Dr Tom Russ, a consultant psychiatrist and director of the Alzheimer Scotland Dementia Research Centre at the University of Edinburgh, who was involved in the trials.

‘With interrupted, bad sleep you don’t get into this [non-REM] stage so don’t go into this clearing process — raising the risk of amyloid build-up,’ says Dr Coulthard.

Other scientists are now investigating whether drugs for insomnia could help prevent dementia or treat early signs of disease.

‘It always makes sense to prevent rather than focus on treating conditions — but we must prioritise both equally,’ says Gill Livingston, a professor of psychiatry of older people at University College London.

The significance of this is borne out by the fact that while the number of people with dementia is increasing — as we have an older population — the rate per 100,000 has decreased considerably, by 25 per cent in 20 years, says Professor Livingston.

The difficulty is that there is a lack of direct evidence from robust clinical trials for lifestyle interventions to prevent dementia, says Dr Sebastian Walsh, an academic clinical fellow at the University of Cambridge, but the emerging evidence is pointing clearly towards a benefit of maintaining a healthy lifestyle (e.g. exercising more, eating well, keeping your brain active), reducing dementia risk.

Also, crucially, many people have this plaque build-up but never develop symptoms of Alzheimer’s, says Dr Russ.

‘But even with amyloid build-up, we still don’t know who will progress to have symptoms of Alzheimer’s and who won’t — so it can’t be the whole story.’.

Indeed, one theory, he says, is that amyloid is a good thing, and may be part of the way the brain adapts to Alzheimer’s, rather than a cause. .

‘We don’t even know what happens long term if we remove amyloid because patients who take the amyloid-lowering drugs are not followed up after studies end,’ adds Professor Howard.

Another option is to vaccinate people against dementia — U.S.

The hope is that this could treat Alzheimer’s and prevent it in people at risk.

‘Trials so far have been targeting amyloid-beta plaque, but this is not a cause of disease but a consequence of it,’ says Mark Carr, a professor of biochemistry and chair of the Antibody-Assisted Drug Discovery Consortium at the university

Using the analogy of measles, he explains that ‘to cure it you don’t treat the spots, you target the virus that causes disease — we identified a rare form of amyloid-beta that causes Alzheimer’s, and when we targeted it using an antibody in mice, we were able to spectacularly slow disease progression’

These studies have also revealed that some patients have lots of tau tangles, and yet no amyloid plaque — with research suggesting that cognitive decline is closely linked to the number and location of tau tangles

Trials into molecules that prevent tau tangles are under way, says Professor Howard, although it remains early days for these