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Fig. 7 | Acta Neuropathologica Communications

Fig. 7

From: Importance of extracellular vesicle secretion at the blood–cerebrospinal fluid interface in the pathogenesis of Alzheimer’s disease

Fig. 7

As a mouse model for Alzheimer’s disease (AD), we injected amyloid beta oligomers (AβO) into the cerebrospinal fluid (CSF) of wild-type (WT) mice via their left lateral brain ventricle (i.e. intracerebroventricular (icv) injection) (Panel A). This resulted in an increased release of extracellular vesicles (EVs) into the CSF, whereby these EVs are at least in part derived from the choroid plexus (CP) (Panel B). Interestingly, AβO-induced, CP-derived EVs carry several pro-inflammatory proteins including the complement protein C3. Furthermore, we could show that the AβO-induced, CP-derived EVs exert a pro-inflammatory response on brain target cells in vitro (panel D). Strikingly, these EVs also play a role in loss of cognitive function (panel C), since blocking the EV secretion using GW4869 protected against the AβO-induced cognitive decline. Image created with BioRender

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