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EFFECT OF NEURAL EXTRACELLULAR VESICLES ON THE MODULATION OF CELL SURVIVAL DURING AGING
Raquel García Rodríguezand 6 co-authors
Centro de Biología Molecular Severo Ochoa (CBM-CSIC)
FENS Forum 2026 (2026)
Barcelona, Spain
Board PS04-08PM-055
Presentation
Date TBA
Board: PS04-08PM-055
Event Information
Poster Board
PS04-08PM-055
Poster
View posterAbstract
Extracellular vesicles (EVs) produced during embryonic development have garnered increasing attention for their roles in coordinating fundamental developmental processes. In parallel, emerging preclinical evidence indicates that EVs derived from young organisms possess significant therapeutic potential for the treatment of adult and injured tissues. In this study, we demonstrate that EVs isolated from the embryonic mouse cerebral cortex and from young mouse cortical neurons in vitro reduce lactate dehydrogenase (LDH) release, enhance mitochondrial respiration, activate Akt signaling, and attenuate the deleterious effects of tumor necrosis factor alpha (TNFα) in in vitro models of neuronal stress, as well as in an in vivo model of retinal degeneration.
Proteomic analysis by mass spectrometry revealed that embryonic EVs are enriched in peptides associated with receptor tyrosine kinase (RTK) signaling, anti-inflammatory responses, and protein synthesis. Notably, among the neurotrophic factors identified, brain-derived neurotrophic factor (BDNF) and insulin were found to be stably associated with the external surface of the vesicles and displayed remarkable stability in activating their respective receptors. Phosphoproteomic profiling of EV-treated cells identified CaMKIIα as a central signaling node, with downstream targets involved in microtubule stabilization, synaptic plasticity, and membrane–cytoskeleton interactions.
Consistent with these molecular findings, embryonic cortex-derived EVs—but not EVs isolated from the cortex of aged mice—significantly enhanced microtubule stability and mitochondrial respiratory capacity in aged neurons. Collectively, these results demonstrate the robust neuroprotective properties of EVs derived from the embryonic mouse cortex and provide insight into the molecular mechanisms underlying their protective effects.
Proteomic analysis by mass spectrometry revealed that embryonic EVs are enriched in peptides associated with receptor tyrosine kinase (RTK) signaling, anti-inflammatory responses, and protein synthesis. Notably, among the neurotrophic factors identified, brain-derived neurotrophic factor (BDNF) and insulin were found to be stably associated with the external surface of the vesicles and displayed remarkable stability in activating their respective receptors. Phosphoproteomic profiling of EV-treated cells identified CaMKIIα as a central signaling node, with downstream targets involved in microtubule stabilization, synaptic plasticity, and membrane–cytoskeleton interactions.
Consistent with these molecular findings, embryonic cortex-derived EVs—but not EVs isolated from the cortex of aged mice—significantly enhanced microtubule stability and mitochondrial respiratory capacity in aged neurons. Collectively, these results demonstrate the robust neuroprotective properties of EVs derived from the embryonic mouse cortex and provide insight into the molecular mechanisms underlying their protective effects.
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