University of Cincinnati researchers have created a pioneering animal model that sheds light on the role a little-understood brain organ plays in repairing stroke damage.

The research was published on July 2 within the journal Proceedings of the National Academy of Sciences and desired to learn more about how the adult brain generates recent neurons to repair damaged tissue.

The research team focused on the choroid plexus, a small organ within the ventricles of the brain that produces cerebrospinal fluid (CSF). CSF circulates throughout the brain, carrying signaling molecules and other aspects regarded as essential for maintaining brain function. Nevertheless, before this study, little was known concerning the role of the choroid plexus and CSF in brain repair after injury on account of the shortage of accessible adult animal models.

“We’ve got discovered a recent use for an animal model that enables us to control the choroid plexus and cerebrospinal fluid in adults for the primary time. Now that we now have discovered this, it is going to be incredibly useful to permit researchers to control the choroid plexus and cerebrospinal fluid in adults to check different disease models and biological processes.”

Agnes (Yu) Luo, PhD, corresponding writer of the study and professor and deputy head of the Department of Molecular and Cell Biology on the University of California School of Medicine

Aleksandr Taranov, a student on the University of California and co-author of the study, explained that in a process called adult neurogenesis, the adult brain retains some ability to repair damage by regenerating newly formed neurons.

“Nevertheless, we still have no idea what actually regulates adult neurogenesis and easy methods to redirect neurons to the positioning of harm after a stroke,” Taranov said.

Using this recent model, the researchers found that removal of the choroid plexus—and the resulting lack of CSF within the brain’s ventricles—led to a discount within the variety of newborn immature neurons called neuroblasts. Within the ischemic stroke model, the team found that lack of the choroid plexus and CSF led to fewer neuroblasts migrating to the positioning of injury and repairing stroke damage.

“This implies that the choroid plexus could also be needed to trap these neuroblasts where they normally are,” Taranov said. “And the choroid plexus may very well be needed to trap neuroblasts in order that they will easily migrate to the stroke site at any time when a stroke or other injury occurs.”

In actual fact, Luo said, the choroid plexus appears to deal with a garrison of regenerative cells which can be able to deploy to damaged brain areas in animal models of stroke. More research is required to verify whether this also happens in human brains.

Taranov is next studying how lack of the choroid plexus and cerebrospinal fluid affects the clearance of toxic proteins in a model of Alzheimer’s disease, and his colleague, graduate student Elliot Wegman, is studying the identical effects in a model of Parkinson’s disease.