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  3. Special Talk with Dr. Anne Desmazieres: Neuronal activity and immune cues modulate neuron-microglia communication at the node of Ranvier, shaping its role in repair
Special Talk with Dr. Anne Desmazieres: Neuronal activity and immune cues modulate neuron-microglia communication at the node of Ranvier, shaping its role in repair
Simons Center for the Social Brain

Special Talk with Dr. Anne Desmazieres: Neuronal activity and immune cues modulate neuron-microglia communication at the node of Ranvier, shaping its role in repair

Add to CalendarAmerica/New_YorkSpecial Talk with Dr. Anne Desmazieres: Neuronal activity and immune cues modulate neuron-microglia communication at the node of Ranvier, shaping its role in repair09/24/2025 2:00 pm09/24/2025 3:00 pmBuilding 46,46-3310, Picower Seminar room
September 24, 2025
2:00 pm - 3:00 pm
Location
Building 46,46-3310, Picower Seminar room
Contact
asokhina@mit.edu
    Description

    Date: Wednesday, September 24, 2025
    Location: 46-3310
    Time: 2:00pm-3:00pm EDT

    *This Special talk is co-hosted by the Picower Institute for Learning and Memory and the Simons Center for the Social Brain

    Speaker: Anne Desmazieres., Ph.D.
    Affiliation: Paris Brain Institute/Institut du Cerveau (ICM), Team Regain in MS

    Talk title: Neuronal activity and immune cues modulate neuron-microglia communication at the node of Ranvier, shaping its role in repair

    Abstract: Multiple Sclerosis (MS) is an inflammatory, demyelinating and neurodegenerative disease of the central nervous system (CNS). While an endogenous repair process exists following demyelination in MS, it is incomplete and varies between individuals. Understanding the mechanisms of remyelination and neuroprotection is therefore crucial to promote repair in patients.

    In MS, the nodes of Ranvier, which support the fast axonal conduction, are disrupted but can reorganize early during repair, even before remyelination proceeds. Furthermore, microglia, the central nervous system resident immune cells, are key players in the disease, as they can engage in pro-inflammatory as well as pro-regenerative processes.

    Our recent work identified nodal structures as a preferential site for microglia-neuron interaction in both mouse and human. We now demonstrate that neuronal activity promotes microglia-node interaction and the switch towards pro-regenerative microglia. Conversely, adaptive immune cues impair microglia-node interaction in an inflammatory MS model and the extent of these interactions at the onset of remission correlates with recovery. Taken together, our findings identify factors that influence microglia-neuron crosstalk in disease and suggest that neuronal activity supports remyelination not only by directly regulating oligodendroglia, but also by modulating microglial behavior during repair.

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