Abstract
The blood-cerebrospinal fluid barrier (CSF) forms a unique interface between blood and brain. It consists of a single cell layer, called choroid plexus epithelium, situated at the interface of blood and CSF. The choroid plexus epithelium has different important functions: it forms a barrier to protect the brain from fluctuations in the blood thereby assuring brain homeostasis, produces CSF and is responsible for the active removal of toxic molecules from the brain. In recent years, the choroid plexus epithelium has gained increasing attention, especially its role in different pathologies. Our mouse studies show that systemic inflammation induces increased blood-CSF barrier leakage and peripheral inflammatory triggers also induce an increase in extracellular vesicle release by the choroid plexus epithelium into the CSF. Strikingly, these choroid plexus-derived EVs are able to enter the brain parenchyma, are taken up by astrocytes and microglia and transfer a pro-inflammatory message to the brain. Moreover, systemic inflammation sensitizes to the development of amyloid beta pathology. In conclusion, we found that peripheral inflammatory triggers affect barrier and secretory activity of the choroid plexus epithelium and influence disease pathology in Alzheimer's disease.
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