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Paranodal destruction and axo-glial dysjunction in a subtype of CIDP with anticontaction-1 antibodies
  1. Satoshi Kuwabara,
  2. Sonoko Misawa,
  3. Masahiro Mori
  1. Department of Neurology, Graduate School of Medicine, Chiba University, Chiba, Japan
  1. Correspondence to Satoshi Kuwabara, Department of Neurology, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba 260-8670, Japan; kuwabara-s{at}faculty.chiba-u.jp

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Myelinated axons have four distinct domains: node, paranode, juxta-paranode and internode. The nodes of Ranvier are the sites where action potentials are generated to sustain saltatory conduction. At the paranodes, the terminal myelin loops are tightly connected to the axolemma by adhesion molecules, such as contactin, contactin-associated protein (Caspr) and neurofascin-155. Detachment of the paranodal myelin terminal loops largely affects nerve conduction; massive leak of driving current from the paranodal region leads to significant reduction of the safety factor for impulse transmission and nerve conduction block.

Such disruption of the axo-glial junction can cause axonal damage by interfering axo-glial interaction. Initially ‘axo-glial dysjunction’ was described in spontaneously diabetic BB-Wistar rats that functionally and structurally model human diabetic neuropathy.1 Reduced Na+ …

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