One research group may have discovered a novel way to eliminate harmful brain proteins that can cause cognitive diseases such as Alzheimer’s disease and Parkinson’s. It could lead to new treatment options for these devastating disorders. 

According to experts, Alzheimer’s disease is caused by the accumulation of amyloid beta protein in the brain. This clumping causes symptoms like memory loss or loss of general cognitive function. 

Research from the Washington University School of Medicine in St. Louis, Missouri, found that ramping up levels of a separate protein — aquaporin 4 — could help to remove them.

In a study on mice genetically-engineered to make more amyloid beta, they found that those given compounds that boosted the levels of aquaporin 4 cleared the harmful proteins faster than those that received a placebo or inert liquid.

Each year around 500,000 Americans get diagnosed with Alzheimer’s. 120,000 people die each year from this disease. The study suggests that having more aquaporin 4 could help prevent the condition — but may not cure it. Scientists have suggested that Alzheimer’s may not be caused by a buildup of beta amyloid. However, it remains unclear what exactly causes the condition.

Scientists at Washington University School of Medicine in St Louis, Missouri, say they have found that ramping up levels of a protein in the brain could clear other proteins that cause dementia

Washington University School of Medicine St. Louis (Missouri) scientists have discovered that raising brain protein levels can clear the way for other proteins that could lead to dementia.

In the study — published Wednesday in the journal Brain — scientists began by studying how aquaporin 4 was made in the brain.

Sometimes, this protein has a little tail at the end.

Initial thought by scientists was that this was a mistake in the way the protein was generated.

Your risk for dementia could be revealed by a heart scan at the end of your life 

Study suggests that heart scans can be used to accurately predict the likelihood of you developing dementia.

Researchers found elderly people with abnormalities in their left atrium were a third more likely to develop the disease — even if they showed no sign of heart problems.

The scans that are usually used only for heart attack victims or people suspected of having heart disease could identify the highest-risk individuals.

The left atrium pumps oxygenated blood to all vital organs and the brain. If the chamber is faulty, it can reduce blood flow to the brain — a risk for dementia.

Arial cardiopathy refers to a range of conditions that may cause the left side of the heart not to function properly.

You may experience strokes and irregular heartbeats. These complications are also possible with dementia.

The study, which included more than 5,000 American adults aged over 70 years old, concluded that atrial heart disease was an “independent risk factor”.

Johns Hopkins University in Baltimore was the lead researcher. He said they could use it to help develop ‘new interventions strategies.

However, research soon revealed that the DNA codes for this mutation were found in multiple species.  

Testing showed that it was also normally around support cells — called astrocytes — which regulate the flow of water and nutrients into the brain from the blood. 

The researchers speculated that the ‘tail’ of the aquaporin 4 was acting as a flap to regulate the flow of nutrients and water through the blood vessels. They suggested that the brain would flush out more amyloid beta if aquaporin 4, which is used to open and close the flap more frequently, was more common.

The theory was tested by raising aquaporin levels in mice that were genetically engineered for more amyloid beta.

Darshan Sapkota (biologist who led the study) screened 2 560 compounds to find out if it was possible to boost the production.

He found two to investigate: Apigenin — normally found in chamomile, parsley, onions and other plants — and sulphaquinoxaline — an antibiotic used by vets.

Participants were divided into two groups: five- or six-legged mice received sulphaquinoxaline and apigenin. A placebo was also administered.

A needle was inserted into each mouse’s brain and connected to a machine to continue the delivery of the drug for approximately 20 hours.

These compounds helped to remove amyloid beta quicker than the ones that didn’t.

The amyloid beta levels of both the groups were measured every hour. However, Dr John Cirrito from Washington University said that they noticed a significant difference within hours.

Cirrito answered’s question about whether results mean people need to rush to purchase onions, chamomile and other high-apigenin plants.

“The results suggest that this is a very special situation. It is known that it has an effect on the beta amyloid, however it could also have an impact on other areas.

Apigenin can be used as a supplement to your diet, however the doctor cautioned against excessive consumption because of unknown effects. 

Consuming the antibiotic sulphaquinoxaline is unsafe for humans. This is a medication that is usually only administered to cattle and sheep in order to treat infection.

Scientists are continuing their work to find other compounds that may be used to reduce amyloid beta levels in the brain. The scientists are looking into ways to inject the compounds directly into the brain without using a needle.

These researchers suggest that human trials may be possible in less than 10 years after more research. 

But scientists are not clear on what causes Alzheimer’s — which affects about six million Americans.

This is because plaques in brains cause damage to cell communication. But some papers suggest that — while this is associated with the condition — it may not actually cause it.

One study by the University of California San Diego that was published on 700 subjects in 2020 suggests amyloid beta may be associated with some of the conditions rather than being the cause.

Dr. Cirrito said: “There are lots of data suggesting that reducing Amyloid levels by 20 percent or 25 percent prevents amyloid accumulation, at least in mice. And the results we observed were within that range.

This tells us that it could be a new approach to Alzheimer’s or other neurodegenerative disorders that affect protein aggregation. 

“There is nothing to indicate that this process applies only to amyloid beta. People with Parkinson’s may benefit from it by increasing alpha-synuclein elimination.

Team members are now investigating drugs that might influence the production aquaporin 4, by looking at compounds such as sulphaquinoxaline.

Sapkota stated, “We’re searching for something that can be quickly translated to the clinic.”

“Just knowing it can be targeted by drugs is an indicator that something exists that we might find useful.”

Part of the National Institute of Neurological Disorders and Strokes funded this research.

Sapkota, who was then a postdoctoral researcher at Washington University and now an assistant professor of biological science at Texas Tech, Dallas, led this study.

Alzheimer’s Disease is currently the most prevalent form of dementia, affecting approximately six million Americans.

The abnormal accumulation of proteins around and in brain cells is believed to cause it, along with amyloid beta. Tau is another factor.

Scientists are not sure why these build up in some people, but it could be linked to genetic factors, diet or a head injury — among others.