Dementia cure hope as scientists discover shock therapy that ‘repairs misfolded proteins’

Dementia cure hope as scientists discover shock therapy that ‘repairs misfolded proteins’

A cure for dementia may have come a step closer after scientists found a way of repairing ‘misfolded’ proteins linked to the condition.

Researchers discovered a ‘shock’ to cells can reverse the abnormal build-up of proteins called amyloid beta in the brain.

When these proteins are misfolded, they end up sticky on the outside and clump together to form plaques – which is thought to kill brain cells and lead to Alzheimer’s disease, a form of dementia.

Scientists found heat shock proteins, which are triggered by high body temperatures, can undo this misfolding.

It could help to explain research showing people who frequently use saunas in Finland are less likely to get dementia.

The team from the UK Dementia Research Institute at the University of Cambridge cautioned that the research, part-funded by the Alzheimer’s Society, is in its early stages.

But Dr Edward Avezov, senior author of the study, said: ‘Optimistically, in the future we could find a drug to awaken this mechanism we have discovered and prevent diseases like dementia.’

Almost a million people in the UK have dementia and there are no drugs to prevent it.

Scientists have struggled to remove amyloid beta clumps in the brain.

The study, published in the journal Nature Communications, identifies a potential means of preventing the build-up.

But shocking could cause stress that kills off brain cells. So experts are searching for a way to provoke a similar reaction in the brain, which could lead to a drug being developed.

Dr Richard Oakley, associate director of research at the Alzheimer’s Society, said the study was a ‘game-changer for dementia research’.

He added that it was a ‘step towards effective and safe treatments’ for people with dementia.

Professor Tara Spires-Jones, from the University of Edinburgh, said: ‘This study adds to previous work which similarly showed stressing cells with cold instead of heat can protect them from misfolded proteins. But a drug which targets these mechanisms is likely to be many years away.’