Microglia rescue neurons from aggregate-induced neuronal dysfunction and death through tunneling nanotubes

Hannah Scheiblich(University Hospital Bonn), Frederik Eikens(University Hospital Bonn), Lena Wischhof(German Center for Neurodegenerative Diseases), Sabine Opitz(University of Bonn), Kay Jüngling(University of Münster), Csaba Cserép(HUN-REN Institute of Experimental Medicine), Susanne V. Schmidt(University Hospital Bonn), Jessica Lambertz(University Hospital Bonn), Tracy Bellande(Commissariat à l'Énergie Atomique et aux Énergies Alternatives), Balázs Pósfai(HUN-REN Institute of Experimental Medicine), Charlotte Geck(University Hospital Bonn), Jasper Spitzer(University Hospital Bonn), Alexandru Odainic(The University of Melbourne), Sergio Castro‐Gomez(University Hospital Bonn), Stephanie Schwartz(University Hospital Bonn), Ibrahim Boussaad(University of Luxembourg), Rejko Krüger(University of Luxembourg), Enrico Glaab(University of Luxembourg), Donato A. Di Monte(German Center for Neurodegenerative Diseases), Daniele Bano(German Center for Neurodegenerative Diseases), Ádám Dénes(HUN-REN Institute of Experimental Medicine), Eike Latz(University Hospital Bonn), Ronald Melki(Commissariat à l'Énergie Atomique et aux Énergies Alternatives), Hans-Christian Pape(University of Münster), Michael T. Heneka(University of Massachusetts Chan Medical School)
Neuron
July 25, 2024
Cited by 158Open Access
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Abstract

Microglia are crucial for maintaining brain health and neuron function. Here, we report that microglia establish connections with neurons using tunneling nanotubes (TNTs) in both physiological and pathological conditions. These TNTs facilitate the rapid exchange of organelles, vesicles, and proteins. In neurodegenerative diseases like Parkinson's and Alzheimer's disease, toxic aggregates of alpha-synuclein (α-syn) and tau accumulate within neurons. Our research demonstrates that microglia use TNTs to extract neurons from these aggregates, restoring neuronal health. Additionally, microglia share their healthy mitochondria with burdened neurons, reducing oxidative stress and normalizing gene expression. Disrupting mitochondrial function with antimycin A before TNT formation eliminates this neuroprotection. Moreover, co-culturing neurons with microglia and promoting TNT formation rescues suppressed neuronal activity caused by α-syn or tau aggregates. Notably, TNT-mediated aggregate transfer is compromised in microglia carrying Lrrk22(Gly2019Ser) or Trem2(T66M) and (R47H) mutations, suggesting a role in the pathology of these gene variants in neurodegenerative diseases.


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