The protein aggregates known as beta-amyloid plaques, which develop in the brains of Alzheimer’s patients, impair numerous brain processes and have the potential to destroy neurons. They may also compromise the blood-brain barrier, a protective buffer between the bloodstream and the brain. Engineers have now created a tissue model that mimics the effects of beta-amyloid on the blood-brain barrier. They have used this model to demonstrate how this damage can allow blood-clotting molecules like thrombin, typically found in the bloodstream, to enter the brain and further harm Alzheimer’s neurons.
The amyloid-beta secreted by Alzheimer’s disease cells can impede barrier function. Once that function is impaired, factors are secreted into the brain tissue that can have detrimental effects on the health of neurons, as the researchers demonstrated clearly in this model.
The researchers also used the tissue model to demonstrate how a drug that improves the blood-brain barrier can lessen cell loss rate in Alzheimer’s disease neurons. Many specialized proteins enable the blood vessel cells that make up the blood-brain barrier to form tight junctions, which are cellular structures that function as a solid seal between cells.
Brain blood vessel injury brought on by beta-amyloid proteins in Alzheimer’s patients is called cerebral amyloid angiopathy. (CAA).
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