Research has shown that the choroid plexus and cerebrospinal fluid are crucial in maintaining a pool of newly generated neurons that aid in repairing the adult brain following injury.
At the University of Cincinnati, researchers have developed an innovative animal model to explore the role of an often overlooked brain organ in the repair of stroke-induced damage.
The study, published on July 2 in the Proceedings of the National Academy of Sciences, aimed to delve deeper into how the adult brain generates new neurons for tissue repair.
The research team concentrated on the choroid plexus, a small organ located within the brain ventricles that produces cerebrospinal fluid (CSF). CSF circulates in the brain, transporting signaling molecules and other essential factors believed to be crucial for maintaining brain function. Despite this, little was known about the role of the choroid plexus and CSF in brain repair post-injury due to a lack of adult animal models.
“We’ve identified a new animal model that enables us to manipulate the adult choroid plexus and CSF for the first time,” stated Agnes (Yu) Luo, PhD, the corresponding author of the study and a professor in UC’s College of Medicine. “This breakthrough will allow researchers to explore different disease models and biological processes by manipulating the adult choroid plexus and CSF.”
UC graduate student and study coauthor, Aleksandr Taranov, explained that through a process known as adult neurogenesis, the adult brain retains the ability to repair damage by producing newly generated neurons.
“However, we are still uncertain about the factors that regulate adult neurogenesis and how to guide neurons to the injury site following a stroke,” Taranov noted.
Using this new model, the researchers observed that removing the choroid plexus, and consequently losing CSF in the brain ventricles, led to a decrease in newly formed immature neurons called neuroblasts. In an ischemic stroke model, the team observed that the absence of the choroid plexus and CSF resulted in fewer neuroblasts migrating to the injury site and aiding in the repair process.
“This indicates that the choroid plexus may play a role in retaining these neuroblasts in their usual habitat,” Taranov explained. “Moreover, the choroid plexus might be necessary for maintaining these neuroblasts so they can migrate efficiently to the site of a stroke or other injuries.”
Luo suggested that the choroid plexus serves as a reservoir of regenerative cells that are primed to be deployed to damaged areas in the brain of animal stroke models. Further research is essential to confirm if this mechanism also occurs in human brains.
Going forward, Taranov is investigating how the absence of the choroid plexus and CSF impacts the clearance of toxic proteins in an Alzheimer’s disease model, while fellow graduate student Elliot Wegman is researching the same effects in a Parkinson’s disease model.
