‘Breakthrough’ investigation finds probable cause

‘Breakthrough’ investigation finds probable causeShare on Pinterest
New research in mice may help open up new treatment options for Alzheimer’s disease. Mascot / Getty Images
  • Worldwide, Alzheimer’s disease is one of the most common forms of dementia.
  • Using mouse models, researchers in Australia have identified one of the probable causes of Alzheimer’s disease. Some have called the finding a “breakthrough.”
  • By studying the blood-brain barrier, researchers have come away with a better understanding of why and how Alzheimer’s disease occurs.
  • Their findings suggest potential treatment and prevention options for the neurodegenerative condition.

The Centers for Disease Control and Prevention (CDC) estimates that up to 5.8 million people in the United States live with Alzheimer’s disease.

Alzheimer’s disease is a neurodegenerative condition that affects parts of the brain associated with memory, thought and language. Its symptoms range from mild memory loss to inability to hold conversations to environmental disturbance and mood swings.

Previous research has suggested that various factors – such as age, family history, diet and environmental factors – are combined to influence a person’s risk of Alzheimer’s disease.

However, researchers in Australia have recently discovered an additional factor that may be responsible for the development of this neurodegenerative condition.

Lead study author Dr. John Mamo, Ph.D. – Senior Professor and Director of the Curtin Health Innovation Research Institute at Curtin University in Perth, Australia – Explained Medical news today the conclusion of the new research.

He said: “To find new ways to prevent and treat Alzheimer’s, we need to understand what is actually causing the disease, and at the moment it has not been determined.”

“This study,” he added, “shows that excessive excess blood of potentially toxic fat-protein complexes can damage microscopic cerebral blood vessels called capillaries and then seep into the brain, causing inflammation and brain cell death.”

β€œ[Changes] in dietary behavior and certain drugs can potentially reduce the blood concentration of these toxic fat-protein complexes, [subsequently] reduce the risk of Alzheimer’s or [slowing] down in disease progression, ”he concluded.

The results appear in the journal PLOS Biology.

Dr. Mamo and his team are working to uncover previously undiagnosed causes of Alzheimer’s disease. Their hope is that this may indicate new pathways of investigation and new potential treatments for the condition.

In their recent study, the researchers used two mouse models. The genetically modified animals in the test group so that their liver would produce human amyloid beta. This is the protein portion of the toxic protein-fat complex that researchers thought could cause Alzheimer’s disease. The control group had no genetic modifications.

Over time, the researchers subjected both groups to a fear-motivated memory test for cognitive functions and noted the corresponding results.

In addition to this test of cognitive function, the researchers harvested various tissue samples from the mice, including samples from the liver, brain, lung and duodenum. This was to investigate the effect of human amyloid beta on the structure and function of these tissues.

When examining the tissue samples or performing the cognitive tests, the researchers did not know if the mouse in question was from the test or control group. This information was only revealed when they were ready to start the statistical analysis of the results. This process is called glare, and it is a research practice that helps reduce the risk of unconscious bias.

The researchers found that when amyloid beta proteins produced in the liver of the test mice combined with fats and traveled to the brain, they disrupted the proper functioning of the brain’s microscopic blood vessels or capillaries.

This dysfunction of the blood-brain barrier caused the protein-fat complexes to leak from the blood into the brain, resulting in inflammation. This inflammation occurred in both the test group and the control group, but it started at a much younger age in the test group.

Unlike in the control group, this inflammation was also associated with marked degeneration in the brain cells of the mice in the test group when examined under a microscope. The researchers only rarely saw this neurodegeneration in the control mice, and it was usually at a much older age.

The team also assessed a marker of neurodegeneration and found that it was approximately twice as large in the test mice than in control mice of the same age.

So it was not surprising that during the test for cognitive function, the test mice performed approximately half as well as the control group in maintaining learning.

These findings suggest explanations for long-standing questions about the role of amyloid beta in the development of Alzheimer’s disease.

Warren Harding, chairman of the board of Alzheimer’s WA, revealed for MNT the significance of the survey results. He said:

“Without significant medical progress such as the breakthrough made by Professor Mamo’s team, it is estimated that the number of Australians living with dementia will exceed 1 million by 2058. […] These findings could have a significant global impact on the millions of people living with Alzheimer’s disease. ”

Limitations of this study include the fact that the researchers performed it only in animal models. This means that despite promising results, further studies – especially in humans – are needed.

Nevertheless, understanding how the amyloid-beta fat complex affects brain capillaries can open up potential medical options for either treating Alzheimer’s disease or slowing the progression of the condition.

Of course, there is a long journey from studies of mice to treatments in humans, but such laboratory research is essential to make the advances necessary to tackle this serious and increasingly common condition.

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