FIGURE 2.

Schematic of different clinical imaging techniques available for investigating the involvement of ChPs in brain disorders. ChP volume and the presence of calcification may be assessed through conventional imaging techniques such as CT and MRI. CSF production may be evaluated with phase-sensitive MRI sequences. ChP capillary perfusion and permeability may be quantified with MRI using dynamic imaging coupled to small molecular weight contrast agents such as gadolinium chelates. Nuclear medicine techniques such as PET give access to: (i) the occurrence of receptors on stromal or epithelial cells (both at the basal or at the apical side) and (ii) epithelial cell metabolism, thanks to dedicated radiotracers. All of these morphological and functional features present a progressive degradation throughout the aging process which might get aggravated in neurological diseases. In addition, in pathological conditions, the extravasation of small molecular weight contrast agents into CSF may allow to image blood-CSF barrier disruption. In inflammatory conditions, reticuloendothelial MRI contrast agents such as iron oxide nanoparticles may get access to the ChP stroma and accumulate into endothelial, stromal, and/or epithelial cells. Alternatively, activation of stromal immune cells (whether resident or infiltrating) may be observed with TSPO-targeted PET radiotracers. Finally, the presence of aggregated proteins due to proteinopathies might be detected with dedicated PET tracers, although this is still debated due to “off-target” binding. ChPs, choroid plexuses; CSF, cerebrospinal fluid; BCSFB, blood-cerebrospinal fluid barrier; MDR, multidrug-resistant; CT, computed tomography; MRI, magnetic resonance imaging; PET, positron emission tomography; TSPO, translocator protein 18 kDa (this figure was prepared with Servier Medical Art).