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- Globally, Alzheimer’s disease is one of the most common forms of dementia.
- Using mouse models, Australian researchers have identified one of the probable causes of Alzheimer’s disease. Some have called the discovery a “breakthrough”.
- By studying the blood-brain barrier, scientists have better understood why and how Alzheimer’s disease occurs.
- Their findings suggest potential options for treating and preventing neurodegenerative disease.
The Centers for Disease Control and Prevention (CDC) estimates that up to
Alzheimer’s disease is a neurodegenerative disease affecting parts of the brain associated with memory, thinking and language. Its symptoms range from mild memory loss and inability to hold conversations to environmental disorientation and mood swings.
Previous research has suggested that various factors – such as age, family history, diet, and environmental factors – combine to influence a person’s risk for Alzheimer’s disease.
However, Australian scientists recently discovered an additional factor that could be responsible for the development of this neurodegenerative disease.
Lead author of the study, Dr John Mamo, Ph.D. – distinguished professor and director of the Curtin Health Innovation Research Institute at Curtin University in Perth, Australia – explained to Medical News Today the conclusion of the new research.
He said: “To find new opportunities for the prevention and treatment of Alzheimer’s disease, we need to understand what really causes the disease, and currently that is not established. “
“This study,” he added, “shows that an exaggerated abundance in the blood of potentially toxic fat-protein complexes can damage microscopic blood vessels in the brain called capillaries and, subsequently, infiltrate the blood. brain, causing inflammation and death of brain cells. “
“[Changes] in eating behaviors and certain drugs could potentially reduce the blood concentration of these toxic fat-protein complexes, [subsequently] reduce the risk of Alzheimer’s or [slowing] the progression of the disease, ”he concluded.
Results appear in the journal PLOS Biology.
Dr Mamo and his team are working to uncover previously unknown causes of Alzheimer’s disease. Their hope is that this may suggest new avenues of investigation and potential new treatments for the disease.
In their recent study, the researchers used two mouse models. They genetically modified the animals in the test group so that their livers produced human beta-amyloid. This is the protein part of the toxic protein-fat complex that scientists believe could cause Alzheimer’s disease. The control group had no genetic modification.
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 cognitive function test, the scientists took various tissue samples from the mice, including samples from the liver, brain, lung, and duodenum. The aim was to study the impact of human beta-amyloid on the structure and function of these tissues.
When examining tissue samples or performing cognitive tests, scientists were unsure whether the mouse in question was in the test or control group. This information was not revealed until they were ready to begin statistical analysis of the results. This process is called blind, and it is a research practice that helps reduce the risk of unconscious bias.
The researchers found that when beta-amyloid proteins made in the livers of the mice tested combined with fat and traveled to the brain, they interfered with the proper functioning of the brain’s microscopic blood vessels, or capillaries.
This dysfunction of the blood-brain barrier caused protein-fat complexes to leak from the blood to 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 the control group, this inflammation was also associated with marked degeneration of brain cells from mice in the test group when examined under a microscope. Scientists rarely saw this neurodegeneration in control mice, and it was usually at a much older age.
The team also evaluated a marker of neurodegeneration and found it to be about twice as important in the mice tested as in the control mice of the same age.
Thus, it was not surprising that during the cognitive function test, the tested mice obtained about half of the performance of the control group in learning retention.
These results suggest explanations for long-standing questions about the role of beta-amyloid in the development of Alzheimer’s disease.
Warren Harding, chairman of the board of directors of Alzheimer’s WA, revealed to MNT the importance of the results of the study. He said:
“Without significant medical advances like the breakthrough made by Professor Mamo’s team, it is estimated that the number of Australians living with dementia will exceed one million by 2058. […] These findings could have a significant global impact on the millions of people living with Alzheimer’s disease.
The limitations of this study include the fact that the researchers only conducted it in animal models. This means that despite promising results, more studies – especially in humans – are needed.
Nonetheless, understanding how the amyloid-beta-fat complex affects brain capillaries may open up potential medical options for treating Alzheimer’s disease or slowing the progression of the disease.
Of course, there is a long journey between studies in mice and treatments in humans, but such lab research is crucial to making the progress needed to tackle this serious and increasingly common disease.
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