Scientists may be able to clear brain of Alzheimer’s-causing proteins


By Luke Andrews Health Reporter for DailyMail.com

16:22 24 Aug 2022, Update 17:22 24 Aug 2022

  • In Alzheimer’s, amyloid beta protein builds up in the brain and sticks together
  • But researchers say they may have found a way to clear them by increasing levels of another protein.
  • In a study on mice genetically engineered to make more amyloid beta, they found compounds that rapidly increase aquaporin 4 levels, cleaving the protein faster.
  • Nearly 500,000 Americans are diagnosed with Alzheimer’s each year

A research team may have discovered a new way to clear harmful proteins in the brain that trigger cognitive diseases such as Alzheimer’s and Parkinson’s, opening the door to new treatments for devastating conditions.

Experts believe that Alzheimer’s begins with amyloid beta proteins forming in the brain and clumping together, triggering telltale symptoms such as memory loss and loss of normal cognitive function.

Research from the Washington University School of Medicine in St. Louis, Missouri found that increasing the levels of a different protein — aquaporin 4 — may help remove them.

In a study on mice genetically engineered to make more amyloid beta, they found that compounds that increased aquaporin 4 levels cleared the harmful protein faster than those that received a placebo or inactive liquid.

About 500,000 Americans are diagnosed with Alzheimer’s each year, and 120,000 die from the disease annually. Studies show that having more aquaporin 4 may help prevent the condition — but it cannot cure it. Although it is not clear what causes Alzheimer’s disease, some scientists suggest that amyloid beta build-up may not be behind it in every case.

Scientists at Washington University School of Medicine in St. Louis, Missouri, say they have found that raising protein levels in the brain can clear out other proteins that cause dementia.

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

Each time this protein is produced with what is described as a ‘short tail’ at the end.

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Initially, scientists thought it was just a fluke due to an error in how the protein was being produced.

Heart scan in old age may reveal your risk of dementia over the next decade

One study suggests that simple heart scans may be able to predict your risk of being diagnosed with dementia within a decade.

Researchers found that abnormalities in the left atrium of elderly people were a third more likely to develop the disease – even though they showed no signs of heart problems.

It suggests that scans typically used only for people with suspected heart disease or heart attacks may help identify who is most at risk of dementia.

The left atrium helps pump oxygen-rich blood to vital organs, including the brain. If the chamber is defective, it can reduce blood flow to the brain — a risk for dementia.

Atrial cardiopathy is the term for a variety of conditions that can cause the left atrium to not work properly.

This can lead to stroke and irregular heartbeat, two complications that have also been linked to dementia.

But a study of more than 5,000 US adults in their 70s concluded that atrial cardiopathy was an ‘independent risk factor’.

Researchers led by Johns Hopkins University in Baltimore said this could help inform ‘new traditional strategies’.

But research quickly revealed that the genes coding for this change were in many different species.

Testing showed that it was also normally around support cells – called astrocytes – that are near blood vessels. He said this is the ‘right place’ if it is used to flush out unwanted substances – such as amyloid beta.

To test the theory, they increased aquaporin 4 levels in mice that were genetically engineered to make more amyloid beta.

Biologist Dr. Darshan Sapkota, who led the study, examined 2,560 compounds that may be able to increase production.

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They found two that may help: apigenin — commonly found in chamomile, parsley, onions and other plants — and sulfaquinoxaline — an antibiotic used by veterinarians.

In the study, rats were administered with either apigenin, sulfaquinoxaline, or a placebo.

The results showed that the compounds that did get cleared amyloid beta faster than those that didn’t.

It was unclear how the substances were given to the mice, whether through supplements or through injections.

Scientists said it is not safe for people to take the antibiotic sulfaquinoxaline without a prescription.

Although apigenin is available as a dietary supplement, he cautioned against consuming too much of it because it is not known how much gets to the brain.

Scientists are now looking for new compounds that will affect the production of aquaporin 4 to be taken into further tests – and eventually human trials if they are shown to be safe.

But scientists aren’t clear what causes Alzheimer’s — which affects about six million Americans.

Amyloid beta build-up in the brain is the prevailing hypothesis, as plaques impair communication between cells. But some papers suggest that – while it is linked to the condition – it cannot actually cause it.

A study published in 2020 on 700 people from the University of California, San Diego is one of those to suggest that amyloid beta was associated with the condition in some cases, rather than the root cause.

Dr. John Sirito, a neurologist involved in the study, said: ‘There is a lot of data that says that reducing amyloid levels by just 20 percent to 25 percent stops amyloid build-up, at least in mice, And the effects we saw were ballpark.

‘This tells me that this could be a new approach for treating Alzheimer’s and other neurodegenerative diseases that involve protein aggregation in the brain.

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‘There is nothing that says this process is specific to amyloid beta. It may also increase alpha-synuclein clearance, which may benefit people with Parkinson’s disease.’

The team is now working on uncovering drugs that may affect the production of aquaporin 4 by looking at sulfaquinoxaline and other compounds.

Sapkota said: ‘We are looking for something that can be translated quickly to the clinic.

‘Just knowing that it’s exactly targeted by a drug is a helpful sign that there’s going to be something out there that we can use.’

The research was funded by the National Institute of Neurological Disorders and Stroke.

Sapkota led the study as a post-doc at the University of Washington, but is now an assistant professor in biological sciences at the University of Texas, Dallas.

Alzheimer’s disease is the most common form of dementia that currently affects approximately six million Americans.

It is thought to be caused by an abnormal buildup of proteins in and around brain cells, including amyloid beta. Others involved are known as Tau.

Scientists aren’t sure why these form in some people, but it may be linked to genetic factors, diet or a head injury — among others.



(This story has not been edited by seemayo staff and is published from a rss feed)

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