ArticleJournal of experimental neurology2026
Extracellular Vesicles in Angelman Syndrome: Expanding UBE3A Role beyond a Cell Autonomous Mechanism.
Article in Journal of experimental neurology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Angelman syndrome (AS) is a severe neurodevelopmental disorder caused by the loss of maternal UBE3A, an E3 ubiquitin ligase essential for neuronal development, synaptic plasticity, and cognitive function. AS has traditionally been viewed as a cell-autonomous disorder in which intracellular UBE3A deficiency drives neuronal dysfunction. However, recent evidence suggests that impaired extracellular vesicle (EV)-mediated intercellular communication also contributes to disease pathophysiology. EVs are key intercellular mediators of neuronal and glial signaling, as they transfer proteins, lipids, and nucleic acids, which regulate synaptic homeostasis, circuit maturation, and brain plasticity. Here, we discuss emerging evidence linking UBE3A deficiency to alterations in EV biogenesis, cargo composition, secretion, and uptake. We propose that disruption of ubiquitin-dependent endosomal trafficking, together with endolysosomal dysfunction involving LAMTOR1 and the lysosomal Ca
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42781634PMC13600349What OpenQuestion holds
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