Tunneling nanotubes between neuronal and microglial cells allow bi-directional transfer of α-Synuclein and mitochondria
Abstract
Tunneling Nanotubes (TNTs) facilitate contact-mediated intercellular communication over long distances. Material transfer via TNTs can range from ions and intracellular organelles to protein aggregates and pathogens. Prion-like toxic protein aggregates accumulating in several disorders, such as Alzheimers, Parkinsons, and Huntingtons diseases have been shown to spread via TNTs not only between neurons, but also between neurons-astrocytes, and neurons-pericytes, indicating the importance of TNTs in mediating neuron-glia interactions. TNT-like structures were also reported between microglia, however their roles in neuron-microglia interaction remain elusive. In this work, we quantitatively characterise microglial TNTs and their cytoskeletal composition, and demonstrate that TNTs form between human neuronal and microglial cells. We show that -Synuclein (-Syn) aggregates increase the global TNT-mediated connectivity between cells, along with the number of TNT connections per cell pair. Homotypic TNTs formed between microglial cells, and heterotypic TNTs between neuronal and microglial cells are furthermore shown to be functional, allowing movement of both -Syn and mitochondria. Quantitative analysis shows that -Syn aggregates are transferred predominantly from neuronal to microglial cells, possibly as a mechanism to relieve the burden of accumulated aggregates. By contrast, microglia transfer mitochondria preferably to -Syn burdened neuronal cells over the healthy ones, likely as a potential rescue mechanism. Besides describing novel TNT-mediated communication between neurons and microglia, this work allows us to better understand the cellular mechanisms of spreading of neurodegenerative diseases, shedding light on the role of microglia.
02 /Specification & Classification
Click any tag to browse matching papers- Organism
- Research Focus
- Approach
Reproducibility ledger
Nobody has reported trying to reproduce this paper yet. Did you replicate an experiment or run the code? Your report saves the next lab a week.
Sign in to file a reproducibility report.
Related papers
- α-Synuclein aggregates induce mitochondrial damage and trigger innate immunity to drive neuron-microglia communication
Ranabir Chakraborty, Stephanie Maya, … Chiara Zurzolo·Nature CommunicationsPeer-reviewed·May 15, 2026
- Neuronal Autophagy Failure Drives α-Synuclein Transfer to Microglia to Outsource Aggregate Clearance
Ranabir Chakraborty, Francesca Palese, … Chiara Zurzolo·Nature CommunicationsPeer-reviewed·Mar 12, 2026
- Common molecular mechanisms underlie the transfer of alpha-synuclein, Tau and huntingtin and modulate spontaneous activity in neuronal cells
Inês Caldeira Brás, Mohammad H. Khani, … Tiago F. Outeiro·bioRxiv·Jul 18, 2021
- Phagocytic glia are obligatory intermediates in transmission of mutant huntingtin aggregates across neuronal synapses
Kirby M. Donnelly, Olivia R DeLorenzo, … Margaret M.P. Pearce·eLifePeer-reviewed·May 28, 2020
- Spreading α-synuclein rewires organelle communication and impairs neuron-astrocyte mitochondrial quality control
Elisabeth Fritsch, Kamelija Horvatović, … Melissa Birol·bioRxiv·Jun 23, 2026
- Quantitative study of alpha-synuclein prion-like spreading in fully oriented reconstructed neural networks reveals non-synaptic dissemination of seeding aggregates
Josquin Courte, Ngoc Anh Le, … Jean‐Michel Peyrin·bioRxiv·Oct 6, 2021