New 'ninja' drug can tackle and diagnose dementia

By: Allison Ward
August 14, 2017

A drug that acts 'like a ninja' could stop the progression of Alzheimer's without causing side-effects.

Scientists are developing the drug that stops beta amyloid protein in the brain from grouping into plaques — one of the main causes of Alzheimer's disease. It has been dubbed the ninja drug because it specifically targets only toxic types of amyloid protein, groups of the beta type, neutralising them without damaging healthy parts of the brain.

Early results suggest the drug — known as PMN310 — is more effective at blocking the spread of these toxic groups than other drugs currently being trialled as Alzheimer's treatments.

Scientists are developing the drug that stops beta amyloid protein in the brain from grouping into plaques — one of the main causes of Alzheimer's disease (file pic)

Tests on mice also found it prevented short-term memory loss and may even reverse symptoms.

Around 850,000 people in the UK have dementia and 62 per cent of those have Alzheimer's disease.

In Alzheimer's, proteins build up within the brain forming either plaques — caused by beta amyloid — or tangles: both kill nerve cells and damage the brain.

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No successful treatment exists for the disease and most drugs tested so far have failed to remove plaques from the brain.

But the 'ninja' drug, developed by Canadian biotech company proMIS, is designed to target Alzheimer's in a different way — by preventing plaque from building up in the first place.

Beta amyloid protein is produced throughout our lifetime as a waste product from the brain's natural processes.

Early results suggest the drug — known as PMN310 — is more effective at blocking the spread of toxic groups than other drugs currently being trialled as Alzheimer's treatments (file pic)

In younger people, the brain can clear out the waste product more quickly than it makes it, but as people age the balance shifts and amyloid begins to build up.

With Alzheimer's, the protein starts grouping and can form plaques which damage nerve cells and eventually kill brain tissue. The disease process can start years before any symptoms show, so experts believe targeting beta amyloid before it turns into plaque could be key to preventing the spread of the disease — and even stop symptoms occurring.

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Researchers from proMIS and the University of British Columbia in Canada designed the PMN310 drug to bind to these toxic beta amyloid groups and stop them from killing nerve cells without damaging any other parts of the brain.

Tests on humans to see if the drug can halt the progression of Alzheimer's are due to start within the next 18 months. In future, the drug could even be used as a way to diagnose Alzheimer's. Early tests showed it binds to toxic amyloid groups in spinal fluid as well as in the brain, meaning it could be used to test whether someone has high levels present in their body — a potential warning sign for Alzheimer's.

Commenting on the drug, Dr Doug Brown, director of research and development at the Alzheimer's Society said: 'This promising study shows the design of a new drug to target amyloid in a different way — removing the groups of amyloid protein that develop before they become plaques.

'Researchers believe this may be more effective and safer than removing the plaques themselves. It's very early days for this drug, and more development will be needed before it can even be tested for safety in people.'

■ Meanwhile, scientists have found people who suffer breathing problems in their sleep are at a 26 per cent higher risk of developing dementia.

Researchers at Wheaton College in the U.S. found those with sleep apnoea had more plaque in their brains and built it up at a faster rate. Sleep apnoea is a condition where the airways close during sleep, temporarily starving the brain of oxygen.

Scientists believe this accelerates damage to the brain and increases the build-up of plaque — a key cause of Alzheimer's.

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Could this be the route to stop tooth decay for good? 

Scientisis have developed a molecule that can prevent or slow down the development of tooth cavities.

The molecule works on Streptococcus mutans, the bacteria responsible for most tooth decay.

It prevents the bacteria forming a sticky biofilm that allows them to bind to the teeth and eat away at them.

In laboratory tests the molecule, which is being likened to a drug, dramatically reduced the incidence of tooth cavities in rats, even when they were fed food likely to encourage decay, according to the journal Scientific Reports.

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Muscle, not the brain, may be targeted in future treatments for sleep disorders. 

This follows a finding that a protein in muscle tissue, known as BMAL1, acts as a body clock, helping regulate the length and depth of our sleep. 

People with higher levels recover from sleep loss faster, reports the journal Elife. 

Want another drink? Try listening to music 

 Could the ability to say no to another drink be as simple as listening to a piece of music?

Scientists at Yale University in the U.S. asked 12 men and women with alcohol addiction to rate their cravings for a drink while listening to music through some headphones.

They then repeated the experiment, but instead played white noise — a hissing sound that has no frequency patterns.

The participants’ desire for a drink was much lower with the music.

The researchers believe that music stimulates the mesolimbic system — the same part of the brain that alcohol and drugs activate.

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Jab to boost heart attack patients

Injections of a protein can boost the heart in a similar way to exercise — and could prevent heart failure, say researchers from Ottawa Hospital.

The heart usually heals badly after a heart attack, becoming overly enlarged and floppy, leading to heart failure, where it can’t pump blood as efficiently as before.

Now a study published in the journal Cell Research has found that injecting a protein called CT1 into a damaged heart encouraged it to repair tissue and grow new blood vessels — increasing the heart’s ability to pump blood — as happens with exercise, said the Canadian researchers, who hope to get approval to test the therapy in humans soon.

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Cattle may protect against lung cancer 

A lifetime spent near cows may help cut the risk of lung cancer later in life by up to 40 per cent, reports the American Journal of Epidemiology.

Exposure to horses has a similar benefit but pigs and chickens offer no protection.Researchers in France tracked 170,000 farm workers over several decades. The longer people worked with cattle, the lower their lung cancer risk.

Earlier studies have found the immune systems of farmers who inhale cow manure particles — which is full of bacteria — are more robust and better able to destroy cancer cells.

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Skin cell that can make insulin 

Skin cells from patients with mature onset diabetes (which is different from either type 1 or type 2) have been transformed into insulin-producing cells. It’s a breakthrough that could spell the end of insulin injections.

Scientists from the University of Bergen in Norway took human skin cells and added chemical compounds to turn them back into stem cells, which have the ability to transform into any cell. According to their study, in the journal Scientific Reports, they then added cells from the pancreas (where insulin is made) of a deceased donor and potassium chloride to trigger the skin cells into making the hormone insulin.

The next step is to get the cells to produce insulin in response to glucose (blood sugar).


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