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Pervasive axonal transport deficits in multiple sclerosis models.

Catherine Diamante Sorbara1, Naomi Elizabeth Wagner2, Anne Ladwig2

  • 1Institute of Clinical Neuroimmunology, Ludwig-Maximilians Universität München, Marchioninistraße 17, 81377 Munich, Germany; Institute of Neuronal Cell Biology, Technische Universität München, Biedersteiner Straße 29, 80802 Munich, Germany.

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Multiple sclerosis (MS) causes reversible axonal transport deficits that precede axon damage and can be treated with anti-inflammatory drugs. Persistent dysfunction in progressive MS may lead to axon dystrophy.

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Area of Science:

  • Neuroscience
  • Cell Biology
  • Pathology

Background:

  • Impaired axonal transport is linked to neurodegeneration in various diseases.
  • Multiple sclerosis (MS) involves progressive axon degeneration, but the role of axonal transport is unclear.

Purpose of the Study:

  • To investigate axonal transport dynamics and microtubule stability in mouse models of MS.
  • To determine if and how axonal transport is affected during MS pathogenesis.

Main Methods:

  • In vivo two-photon imaging was used to directly observe organelle transport and microtubule stability in spinal axons.
  • Mouse models of acute and progressive MS were utilized.

Main Results:

  • Widespread axonal transport deficits were observed, preceding structural axon changes.
  • These deficits were reversible with acute anti-inflammatory treatments or redox scavenging.
  • In progressive MS models, sustained transport dysfunction led to reduced organelle supply and potential axonal dystrophy.

Conclusions:

  • Acute neuroinflammation in MS induces reversible axonal dysfunction correlating with disease symptoms.
  • Perpetuated transport deficits in advanced MS contribute to axonal dystrophy by impairing distal organelle supply.