Beta-amyloid plaques, the protein aggregates that form in the brains of Alzheimer’s patients, disrupt many brain functions and can kill neurons.
Beta-amyloid plaques, the protein aggregates that form in the brains of Alzheimer’s patients, disrupt many brain functions and can kill neurons. They can also damage the blood-brain barrier — the normally tight border that prevents harmful molecules in the bloodstream from entering the brain.
MIT engineers have now developed a tissue model that mimics beta-amyloid’s effects on the blood-brain barrier, and used it to show that this damage can lead molecules such as thrombin, a clotting factor normally found in the bloodstream, to enter the brain and cause additional damage to Alzheimer’s neurons.
“We were able to show clearly in this model that the amyloid-beta secreted by Alzheimer’s disease cells can actually impair barrier function, and once that is impaired, factors are secreted into the brain tissue that can have adverse effects on neuron health,” says Roger Kamm, the Cecil and Ida Green Distinguished Professor of Mechanical and Biological Engineering at MIT.
Read more at Massachusetts Institute of Technology
Image: The blood-brain barrier — the normally tight border that prevents harmful molecules in the bloodstream from entering the brain — can be damaged by the protein aggregates that form in the brains of Alzheimer’s patients. CREDIT: Christine Daniloff, MIT
