Study finds the likely cause of Alzheimer's disease

The abundance of potentially toxic fat-protein complexes in the blood can damage microscopic brain blood vessels causing inflammation and brain cell death, according to a new study on Alzheimer's disease.

The researchers of Curtin Health Innovation Research Institute at Curtin University in Perth, Australia, found that complexes around toxic fat-protein in the brain damages brain blood vessels called capillaries and leak into the brain, resulting in inflammation.

Lead study author Dr John Mamo 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."

In order to do that Dr Mamo and his team used two mouse models in their study, where they genetically modified animals in the test group so that their livers would produce human amyloid-beta, the protein part of the toxic protein-fat complex that the scientists thought may cause Alzheimer's disease. The control group had no genetic modifications.

They collected various tissue samples from the mice, including samples from the liver, brain, lung, and duodenum to study the impact of the human amyloid-beta on the structure and function of these tissues.

It was found that when the amyloid-beta proteins made in the liver of the test mice combined with fats and travelled 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.

Dr Mamo said, "[Changes] in dietary behaviours 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.

Limitations of this study include the fact that the researchers only conducted it in animal models, which means that despite promising results, further studies — especially in humans — are necessary.

Nevertheless, understanding how the amyloid-beta-fat complex affects brain capillaries may open up potential medical options to either treat Alzheimer's disease or slow down the condition's progression.