The Centers for Disease Control and Prevention (CDC) estimate that up to 5.8 million peopleTrusted Source in the United States live with Alzheimer’s disease.
Alzheimer’s disease is a neurodegenerative condition affecting parts of the brain associated with memory, thought, and language. Its symptoms range from mild memory loss to the inability to hold conversations to environmental disorientation and mood changes.
Previous research has suggested that various factors — such as age, family history, diet, and environmental factors — combine to influence a person’s risk of Alzheimer’s disease.
However, scientists 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. — distinguished professor and director of the Curtin Health Innovation Research Institute at Curtin University in Perth, Australia — explained to Medical News Today the conclusion from the new research.
He said, “To find new opportunities to prevent and treat Alzheimer’s, we need to understand what actually causes the disease, and presently that is not established.”
“This study,” he added, “shows that exaggerated abundance in blood of potentially toxic fat-protein complexes can damage microscopic brain blood vessels called capillaries and, thereafter, leak into the brain, causing inflammation and brain cell death.”
“[Changes] in dietary behaviors and certain medications could potentially reduce blood concentration of these toxic fat-protein complexes, [subsequently] reducing the risk for Alzheimer’s or [slowing] down the disease progression,” he concluded.
The findings appear in the journal PLOS Biology.
What the results say
The researchers found that when the amyloid-beta proteins made in the liver of the test mice combined with fats and traveled to the brain, they interfered with the proper functioning of the brain’s microscopic blood vessels, or capillaries.
This dysfunction in the blood-brain barrier led to the protein-fat complexes leaking 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 scientists 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 it to be approximately two times greater in the test mice than in control mice of the same age.
So, it was unsurprising that during the test for cognitive function, the test mice performed approximately half as well as the control group at retention of learning.
These findings suggest explanations to long standing questions about the role of amyloid-beta in Alzheimer’s disease development.
Warren Harding, board chairman of Alzheimer’s WA, revealed to MNT the significance of the study results. He said:
Article culled from MedicalNewsToday