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UNCOVERING THE ROLE OF EXTRACELLULAR VESICLES IN VPS13A DISEASE: INSIGHTS INTO INTERCELLULAR COMMUNICATION
Gisela Besaand 6 co-authors
Universitat de Barcelona
FENS Forum 2026 (2026)
Barcelona, Spain
Board PS07-10AM-183
Presentation
Date TBA
Board: PS07-10AM-183
Event Information
Poster Board
PS07-10AM-183
Poster
View posterAbstract
VPS13A disease is an ultra-rare inherited neurodegenerative disorder caused by mutations in the VPS13A gene, leading to loss of the VPS13A protein, a bulk lipid transporter. Its absence results in selective, progressive neurodegeneration of the striatum and dysfunction of the corticostriatal pathway and impaired synaptic transmission. In neurodegenerative processes, evidence suggests that disruptions in intercellular communication mediated by extracellular vesicles (EVs) may contribute to impaired signaling. In VPS13A disease, EV dysfunction may underlie synaptic abnormalities and altered corticostriatal communication.We characterized the VPS13A- knockout (KO) effects on neuronal structure and synaptic connectivity on primary neuronal cultures. VPS13A-KO neurons showed reduced neurite length and spine density compared to wild-type (WT) neurons. EVs were then isolated from the culture media of cortical and striatal primary neurons derived from WT and VPS13A-KO mice and characterized by concentration, size distribution, and protein markers. We found that striatum-derived EVs were smaller than cortex-derived EVs. No significant differences were observed between WT- and KO-derived EVs from cortical neurons. In contrast, striatal VPS13A-KO neurons released a lower concentration of EVs compared with WT neurons. Functional studies revealed that treatment of WT neurons with KO-derived EVs reduced neurite area, whereas treatment of VPS13A-KO neurons with WT-derived EVs rescued neurite area. Together, these results suggest that EVs may play a role in the neuropathology of VPS13A disease and highlight their potential role in modulating circuit integrity. Ongoing studies aim to further characterize EVs cargo alterations caused by VPS13A loss and their contribution to synaptic transmission deficits.
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