Tissue model in laboratory reveals role of blood-brain barrier in Alzheimer’s disease

A tissue model that mimics the effects of beta-amyloid plaques, those protein aggregates are known to be a leading cause of Alzheimer’s disease, on the blood-brain barrier was developed by a group of engineers at the Massachusetts Institute of Technology.

The scientists, who then published a study in Advanced Science, showed the damage that beta-amyloid plaques do to this area of the brain. This damage causes harmful molecules in the bloodstream to enter the brain. In particular, researchers have shown that thrombin, a coagulation molecule normally present in the bloodstream, can enter the brain and damage neurons because of this damage.

Roger Kamm, a professor of mechanical and biological engineering at MIT and one of the authors of the study, explains the results his group obtained as follows: “We were able to clearly demonstrate in this model that beta-amyloid released from Alzheimer’s disease cells can actually compromise barrier function and, once compromised, factors are released into brain tissue that can have negative effects on the health of neurons.”

Kamm and his colleagues, including Rudolph Tanzi, a professor of neurology at Harvard Medical, began working on the project several years ago with other researchers at Massachusetts General Hospital. They grew large amounts of beta-amyloid proteins in the laboratory and at the same time developed brain endothelial cells, those cells that form the blood-brain barrier.

These two types of tissue, after 10 days of cellular growth, were connected by collagen. At this point, the researchers discovered that within 3-6 days the molecules could spread from one culture to another. In particular, the beta-amyloid proteins secreted by the neurons began to accumulate in the endothelial tissue which caused the breaking of the blood-brain barrier and allowed thrombin to pass from the blood into the Alzheimer’s neurons leading to their death.

“We were able to demonstrate this bi-directional signaling between cell types and actually solidify things that had previously been seen in animal experiments, reproducing them in a model system that we can control with much more detail and better fidelity,” notes Kamm himself, who adds that this new platform could offer new possibilities with regard to the treatment of Alzheimer’s.


Links/Sources:

https://onlinelibrary.wiley.com/doi/full/10.1002/advs.201900962

Phil Coleman

Phil is a former professor and mathematician with particular expertise in elliptic curves and number theory. During his spare time, he enjoys flicking through science journals and keeping up to date with developments in a number of fields. It's no surprise that he is a valuable and keen contributor to IBN News, and he hopes to build up this publication into 2020 and beyond.

812 Griffin Street, Phoenix Arizona, 85003
602-281-4803
[email protected]
Phil Coleman