Astrocyte - BBB supporter

Now, in a study with potential impacts on a variety of neurological diseases, Virginia Tech researchers have provided the first experimental evidence from a living organism to show that an abundant, star-shaped brain cell known as an astrocyte is essential for blood-brain barrier health.

Furthermore, the finding gives scientists a path to understand diseases where frequent blood-brain barrier damage occurs, including traumatic brain injury, stroke, epilepsy, Alzheimer's disease, and Parkinson's disease.

"Blood-brain barrier leakage is a problem in the aging brain as well as many different neurological diseases,"

 "Without astrocytes, the blood-brain barrier becomes leaky and ineffective, leaving brain tissue vulnerable to a variety of medical conditions. If we know what maintains the barrier in the healthy brain, we will be able to better understand what goes wrong in traumatic brain injury and in Alzheimer's disease—all health problems with blood-brain barrier damage."

Generally, researchers suspect astrocytes support the blood-brain barrier by releasing factors helpful to maintaining tight connections between the cells in the barrier.

The researchers used small, intermediate-sized, and large molecular tracers to evaluate the permeability of the blood-brain barrier. All of the markers passed through the barrier in some areas, while in other areas only small tracers leaked, suggesting that leakages were happening at various sizes.

In recent years, contradictory studies have emerged in which scientists removed astrocytes in animal models with no indications of harm to the blood-brain barrier.

However, when Virginia Tech scientists used a mouse model to mimic the effect of the removal of astrocytes, varying degrees of permanent blood-brain barrier damage occurred, with the amount of damage possibly in proportion with the numbers of ablated astrocytes. In these scenarios, the scientists determined neighboring astrocytes do not rescue the blood-brain barrier when it is damaged.

 

reference

GLIA, onlinelibrary.wiley.com/doi/abs/10.1002/glia.23908