We are pleased to announce that Prof. Efrat Levy (New York University Grossman School of Medicine, USA) will join Targeting Extracellular Vesicles 2026 as a speaker.

Introduction: Mitochondrial components are released into the brain extracellular space via several mechanisms, including mitovesicles. In aging and neurodegenerative disorders, mitochondrial dysfunction alter mitovesicle number and content. Our studies suggested that mitovesicle secretion eliminates detrimental mitochondrial materials from the cell, especially when other mitochondrial quality control mechanisms are disrupted, and that shuttling from one cell to another, dysfunctional mitovesicles transfer this mitochondrial content from a single focal site to the rest of the brain.

Materials and Methods: A) EVs were isolated from the brain of mice expressing human mutated b amyloid precursor protein (APP), prior to Ab aggregation, and age-matched littermate controls. Coronal hippocampal slices from wild-type mice were perfused with subtypes of brain EVs, and long-term potentiation (LTP) recorded. B) Neuronal Neuro-2a cells were incubated with different subtypes of EVs and investigated for mitovesicle uptake and mitochondrial morphology.

Conclusions: Mitovesicles isolated from brains of APP mice perturbed LTP of normal mouse hippocampi, and induced mitophagy and mitoaggresome formation in Neuro-2a cells, revealing that mitovesicles acquire pathogenic functions under conditions of mitochondrial dysfunction, propagating neuropathology and affecting synaptic function. Thus, mitovesicles arise as active players in the brain extracellular milieu, contributing to memory formation deficiencies typically found in Alzheimer’s disease.