Cell adhesion molecules play an important role in the organization of the myelin and of the axonal domains. We have recently shown that autoantibodies against cell adhesion molecules (Neurofascin-155, neurofascin-186, contactin-1, and caspr1) are associated with subgroup of patients with inflammatory demyelinating neuropathies. These cell adhesion molecules play important role in myelin insulation and in the formation of the nodes of Ranvier. These autoantibodies are pathogenic and disorganize the nodal and paranodal domains. Of interest, these autoantibodies are associated with specific subgroups of patients and can serve as diagnostic tools and for treatment orientation.
The mechanisms leading to conduction abnormalities is still unknown in the vast majority of patients with inflammatory neuropathies. Our main goals are to identify the pathogenic mechanisms leading to conduction loss in human demyelinating pathologies, identify novel diagnostic biomarkers, and determine the function of myelin proteins.
Our approaches rely on:
- Neuronal and glial primary cultures
- Proteomic approaches
- Animal models and passive transfer models
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Judith Melki (Kremlin-Bicetre, Paris, France)
Nobuhiro Yuki (Dokkyo medical University, Tochigi, Japan)
Elior Peles (Weizmann Institute, Rehovot, Israël)
Shahram Attarian (Hôpital de la Timone, Marseille, France)
Laurent Aniksztejn (INMED, Marseille, France)
Jean-Michel Vallat (CHU de Limoges, Limoges, France)