WASHINGTON (Dispatches) -- A new study shows how the Alzheimer's disease allows toxins to pass through the blood-brain barrier, further harming neurons.
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.
The researchers also used the tissue model to show that a drug that restores the blood-brain barrier can slow down the cell death seen in Alzheimer's neurons.
The blood vessel cells that make up the blood-brain barrier have many specialized proteins that help them to form tight junctions -- cellular structures that act as a strong seal between cells.
Alzheimer's patients often experience damage to brain blood vessels caused by beta-amyloid proteins, an effect known as cerebral amyloid angiopathy (CAA). It is believed that this damage allows harmful molecules to get into the brain more easily.