Scientists at MIT and MGH have gained new clues into the role of the brain’s blood-brain barrier in Alzheimer’s disease. Recent research has found that damage from Alzheimer’s allows toxins to enter the brain, further harming neurons.
The results are being used to try and develop new drugs to solidify the blood-brain barrier.
The report in MIT News describes how beta-amyloid plaques, the protein aggregates that form in the brains of Alzheimer’s patients, disrupt many brain functions and can kill neurons. Rudolph Tanzi of Milton, a professor of neurology at Harvard Medical School and Massachusetts General Hospital, is one of the senior authors.
The plagues can also damage the blood-brain barrier — the normally tight border that prevents harmful molecules in the bloodstream from entering the brain.
Writing in the MIT News, Anne Trafton of the MIT News Office states that engineers developed a tissue model that mimics beta-amyloid’s effects on the blood-brain barrier. They 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,” said Roger Kamm, the Cecil and Ida Green Distinguished Professor of Mechanical and Biological Engineering at MIT.