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LDN, Endosomes, and the Nanophysiology of Autoimmune Movement Disorders


Mark Cooper, PhD


To discuss the actions LDN, combined with other therapies, to treat autoimmune movement disorders. 

Session Learning Objective:

euroinflammatory lesions correspond, in part, to the functional lesions that underlie certain autoimmune neurological disorders. Close connections between neuroinflammation, neuroautoimmunity, and pain/autonomic/movement disorders are now well established.  Neuroinflammatory lesions can be directly visualized through PET scans, or detected indirectly by abnormal pro-­‐inflammatory cytokine profiles and/or neuroautoantibodies in bodily fluids.  Effective therapies for neuroinflammatory disorders require an understanding of how neuroinflammatory lesions are established and maintained.  This problem involves conceptualizing neuroinflammatory lesions as altered states of intercellular communication, within networks of neurons, glia, endothelial cells, and components of the circulatory immune system (leukocytes, autoantibodies, and complement proteins), which can cross into the nervous system through extravasation. 

The central nervous system utilizes a variety of primary signaling pathways to activate neuroimmune responses.  Inhibition/attenuation of upstream Toll-­‐like receptors (TLRs), purine receptors (P2Rs), and phosphatidylinositol-­‐linked pro-­‐inflammatory pathways are among urrent strategies for the treatment of neuroinflammatory lesions.   Positive outcomes for neuroinflammatory movement disorders (e.g. fixed and paroxysmal dystonias) have been obtained when LDN (low-­‐dose naltrexone) is used in combination with other anti-­‐neuroinflammatory agents, to reset hyperexcitable cellular states, which drive neuropathic pain and movement disorders.  This talk will examine how LDN can be potentially combined with other therapies to help restore normal synaptic tone within the inflamed nervous system, and treat neuroinflammation-­‐linked movement disorders. This discussion will center on the nanophysiology of the endosomal compartment, as well as how signaling from autoimmune-­‐endosomes is likely altered by LDN. 

Session Outline:

-­‐ Neuro-­‐autoantibodies and their targets 
-­‐ Neuroinflammatory pathways affecting sensory-­‐motor circuits 
-­‐ Accumulation of autoantibodies within endosomal compartments 
-­‐ Axonal transport and transcytosis of autoantibodies within endosomes 
-­‐ Attenuating autoimmune movement disorders using LDN and other agents