Alzheimer’s symptoms could be reversed by restoring protein in brain

Alzheimer’s symptoms could be reversed by restoring protein in brain




Alzheimer’s symptoms could be reversed by restoring a protein which is missing in the brains of dementia sufferers, a new study suggests.

Researchers at the University of Glasgow and the Hong Kong University of Science showed that upping levels of the protein IL-33 mobilises the immune system into clearing out amyloid in the brains of mice.

When too much amyloid builds up in the brain, it forms sticky plaques which prevent brain cells form talking to each other.


It had already been established that the brain of patients withAlzheimer's contains less of the IL-33 protein than the brain of non-sufferers.

When the protein was injected into the brains of mice withAlzheimer’s-type disease their memory and brain function rapidly improved within one week.

Glasgow professor Eddy Liew, who co-directed the research, said: "The relevance of this finding to human Alzheimer's is at present unclear. But there are encouraging hints.

“There have been enough false 'breakthroughs' in the medical field to caution us not to hold our breath until rigorous clinical trials have been done. Nevertheless, this is a good start."

The protein also prevents inflammation in the brain tissue, which is associated with deposits and tangles forming in the first place.

There are currently 850,000 people living with dementia in Britain which is due to rise to one million by 2025 and two million by 2050. But there are currently no treatments to prevent or reverse dementia.

Prof Martin Rossor, NIHR National Director for Dementia Research,University College London Hospitals (UCLH), said:

“This study is important as it provides another route to reducing the amyloid protein that is thought to be damaging in Alzheimer’s disease.

“However, there have been many early successes in treating mice that have been genetically modified to produce amyloid deposits but unfortunately these have not transferred to success in treating patients.”

Dr James Pickett, Head of Research at Alzheimer’s Society, said: “Here, the researchers have shown that the protein can lead to short-term improvements in memory and reductions in the amount of amyloid in the brains of mice with symptoms similar to Alzheimer’s disease.

“With an ageing population and no new dementia drugs in over a decade, the need to find treatments that can slow or stop the disease progression is greater than ever.”

The research was published in the Proceedings of the National Academy of Sciences.



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