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Scientists lead the way in race to find new brain disease drug

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Scientists in Cambridge identify gene pattern that could lead to a drug to prevent Alzheimers in thos people thought to be at risk.
Scientists in Cambridge identify gene pattern that could lead to a drug to prevent Alzheimers in thos people thought to be at risk.

Breakthrough could lead to neurostatin for Alzheimer sufferers

Cambridge researchers have made a major breakthrough in the fight to cure Alzheimer’s disease.

Scientists at the University of Cambridge believe a gene signature in healthy brains echoes the same pattern which sees the disease spread in older people.

The discovery was revealed in the journal Science Advances, and could be used to produce preventative treatments for at-risk people long before the symptoms appear.

Researchers found that the body’s defences against a specific group of genes were weaker and that healthy people with the same profile were highly likely to develop the disease in later life.

Alzheimer’s disease, the most common form of dementia, is characterised by the progressive degeneration of the brain.

The disease is currently incurable and its molecular origins are still unknown.

Senior author, Professor Michele Vendruscolo of the Centre for Misfolding Diseases at Cambridge’s Department of Chemistry, said: “What we’ve tried to do is to predict disease progression starting from healthy brains.

““If we can predict where and when neuronal damage will occur, then we will understand why certain brain tissues are vulnerable, and get a glimpse at the molecular origins of Alzheimer’s disease.”

One of the hallmarks of the disease is the build-up of protein deposits, known as plaques and tangles, in the brains of affected individuals.

Dr Vendruscolo added: “We wanted to know whether there is something special about the way these proteins behave in vulnerable brain tissue in young individuals, long before the typical age of onset of the disease.”

Through the analysis of more than 500 samples of healthy brain tissues from the Allen Brain Atlas, they identified a signature of a group of genes in healthy brains and found the same pattern in people suffering from the disease.

He added: “Vulnerability to Alzheimer’s disease isn’t dictated by abnormal levels of the aggregation-prone proteins that form the characteristic deposits in disease, but rather by the weaker control of these proteins in the specific brain tissues that first succumb to the disease,” said Vendruscolo.

Earlier this year, the same researchers behind the current study identified a possible ‘neurostatin’ that could be taken by healthy individuals in order to slow or stop the progression of Alzheimer’s disease.

The latest results suggest a way to exploit the gene signature to identify those individuals most at risk and those who would most benefit from taking a neurostatin in earlier life.

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