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Updated: Dec 25, 2025

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RNA-binding protein altered expression and mislocalization in MS.

Katsuhisa Masaki1, Yoshifumi Sonobe1, Ghanashyam Ghadge1

  • 1From the Department of Neurology (K.M., Y.S., G.G., R.P.R.) and Department of Pathology (P.P.), University of Chicago Medical Center, IL; Neuroimmunology Research Laboratory (P.L., S.Z., A.P.), Centre du Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM), QC, Canada; and Neuroimmunology Unit (F.P., Q.-L.C., J.P.A.), Montreal Neurological Institute, McGill University, QC, Canada.

Neurology(R) Neuroimmunology & Neuroinflammation
|March 29, 2020
PubMed
Summary
This summary is machine-generated.

RNA-binding proteins (RBPs) like TDP-43 and PTB show altered localization in multiple sclerosis (MS) lesions. These changes in oligodendrocytes and neurons may contribute to MS pathogenesis and neurodegeneration.

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Pathology

Background:

  • Altered nuclear localization of RNA-binding proteins (RBPs) is implicated in neurodegenerative diseases like ALS.
  • Specific RBPs, including TDP-43 and PTB, are crucial for cellular function and neuronal development.
  • Theiler murine encephalomyelitis virus (TMEV) infection in oligodendrocytes causes demyelination associated with RBP mislocalization.

Purpose of the Study:

  • To investigate nuclear depletion and mislocalization of TDP-43, FUS, and PTB in MS lesions.
  • To examine these RBPs in human oligodendrocytes under metabolic stress in vitro.
  • To determine if RBP alterations in MS mirror those seen in ALS and TMEV infection.

Main Methods:

  • Analysis of MS lesions for TDP-43, FUS, and PTB localization and expression.
  • In vitro culture of primary human brain-derived oligodendrocytes.
  • Induction of metabolic stress (low glucose/nutrients) in cultured oligodendrocytes.

Main Results:

  • Mislocalized TDP-43 observed in oligodendrocytes within active MS lesions.
  • Decreased PTB1 expression in oligodendrocytes and decreased nuclear PTB2 in neurons in MS lesions.
  • Nuclear depletion of TDP-43 in oligodendrocytes under metabolic stress conditions.
  • FUS mislocalization was not explicitly detailed in the provided results.

Conclusions:

  • Altered expression and mislocalization of TDP-43 and PTB in MS lesions may contribute to demyelination and neurodegeneration.
  • TDP-43 is vital for oligodendrocyte function, while PTB is important for neuronal differentiation.
  • Targeting nucleocytoplasmic transport pathways could be a therapeutic strategy for MS.