Role of Blood-Brain Barrier in Alzheimer's
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.
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.