Related Experiment Video
Updated: Oct 24, 2025
06:45
Microdissection and Whole Mount Scanning Electron Microscopy Visualization of Mouse Choroid Plexus
Published on: December 16, 2022
4.9K
Oxidized/deamidated-ceruloplasmin dysregulates choroid plexus epithelial cells functionality and barrier properties
Alan Zanardi1, Marco Barbariga1, Antonio Conti1
1Proteome Biochemistry, IRCCS-Ospedale San Raffaele, 20132 Milan, Italy.
Neurobiology of Disease
|August 13, 2021
Summary
Oxidized ceruloplasmin in Parkinson's disease (PD) damages the blood-CSF barrier by affecting choroid plexus cells. This damage worsens the disease's pathological processes and alters cerebrospinal fluid composition.
Area of Science:
- Neuroscience
- Cell Biology
- Biochemistry
Background:
- Choroid plexus epithelial cells (CPEpiCs) maintain cerebrospinal fluid (CSF) composition and form the blood-CSF barrier (BCSFB).
- In Parkinson's disease (PD), CSF ceruloplasmin becomes oxidized and deamidated (Cp-ox/de), gaining integrin-binding properties.
Purpose of the Study:
- To investigate the effects of Cp-ox/de on CPEpiCs functions.
- To elucidate the role of Cp-ox/de in altering BCSFB integrity in PD.
Main Methods:
- In vitro studies using CPEpiCs.
- Analysis of cell adhesion, intracellular signaling, proliferation, and secretome.
- Assessment of barrier integrity under oxidative conditions.
Main Results:
- Cp-ox/de binds to CPEpiCs via RGD-recognizing integrins, inhibiting proliferation and altering the secretome.
- Oxidative conditions induce CPEpiCs barrier leakage, allowing Cp-ox/de to cross and signal through integrins.
- This exacerbates BCSFB dysfunction.
Conclusions:
- Cp-ox/de disrupts CPEpiCs function and compromises BCSFB integrity.
- This mechanism contributes to CSF alteration and PD pathogenesis.
- Targeting Cp-ox/de interactions may offer therapeutic strategies for PD.
