Groundbreaking research from Australian scientists has revealed a likely cause of Alzheimer’s disease, the devastating condition that affects 5.8 million Americans. Using mouse models, the researchers built upon previous knowledge of beta-amyloid protein, already known to play a role in Alzheimer’s. They discovered how this toxic protein leaks through the blood-brain barrier to causes degenerative damage to brain cells.

According to Medical News Today, the findings have been called a “breakthrough,” and could lead to preventive strategies to delay the onset of Alzheimer’s disease or slow its progression.

“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,” said lead author Dr. John Mamo, director of the Curtin Health Innovation Research Institute in Perth, Australia. “The study shows that exaggerated abundance in blood of potentially toxic fat-protein complexes can damage microscopic brain blood vessels and, thereafter, leak into the brain causing inflammation and brain cell death.”

The groundbreaking research that appeared two weeks ago in the prestigious journal PLOS Biology, helps uncover the role of beta-amyloid proteins in the development of Alzheimer’s disease, the most prevalent form of dementia globally, and may open additional avenues to prevent and treat the dreaded disease in the future.

“While we previously knew that the hallmark feature of people living with Alzheimer’s disease was the progressive accumulation of toxic protein deposits within the brain called beta-amyloid, researchers did not know where the amyloid originated from, or why it deposited in the brain.” Mamo said in a press release. “Our research shows that these toxic protein deposits that form in the brains of people living with Alzheimer’s disease most likely leak into the brain from fat carrying particles called lipoproteins.”

Mamo and his team genetically altered one group of mice so that their livers produced human beta-amyloid. This is the protein part of the protein-fat complex believed to trigger Alzheimer’s disease, says MNT. The control group had no genetic modifications. Over time, the researchers conducted cognitive tests and found that the test mice performed poorly at an earlier age compared to the control group. 

They also examined tissue samples from the brains and livers of the mice. When the beta-amyloid proteins combined with fats and traveled to the brain, they caused dysfunction in the capillaries that led to leakage from the blood into the brain, resulting in inflammation. The researchers measured a marker of neurodegeneration and found it was two times greater in the test mice than in the control group of mice of the same age, says MNT.

Mamo said that this “blood-to-brain” pathway is a significant discovery “because if we can manage the levels in blood of lipoprotein amyloid and prevent their leakage into the brain, this opens up potential new treatments to prevent Alzheimer’s disease and slow memory loss.”

He added that while further studies are now needed, “this finding shows the abundance of these toxic proteins in the blood could potentially be addressed through a person’s diet and some drugs that could specifically target lipoprotein amyloid, therefore reducing their risk or slowing the progression of Alzheimer’s disease.”