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Related Concept Videos

Glial Cells01:04

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Related Experiment Video

Updated: Jun 12, 2026

An Ex vivo Model of an Oligodendrocyte-directed T-Cell Attack in Acute Brain Slices
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A lymphocyte-microglia-astrocyte axis in chronic active multiple sclerosis.

Martina Absinta1,2,3, Dragan Maric4, Marjan Gharagozloo5

  • 1Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, USA. mabsint1@jhmi.edu.

Nature
|September 9, 2021
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Summary

Chronic demyelination in multiple sclerosis (MS) lesions involves ongoing neurodegeneration. Targeting complement component 1q (C1q) offers a potential therapeutic strategy for this white matter inflammation.

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Last Updated: Jun 12, 2026

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Published on: November 17, 2020

Area of Science:

  • Neuroimmunology
  • Neurodegeneration
  • Magnetic Resonance Imaging (MRI)

Background:

  • Persistent multiple sclerosis (MS) lesions exhibit ongoing demyelination and axon degeneration.
  • Paramagnetic rim lesions on MRI indicate non-resolving MS lesions with active pathology.

Purpose of the Study:

  • To elucidate mechanisms of chronic neurodegeneration in MS lesions.
  • To identify novel therapeutic targets for progressive MS.

Main Methods:

  • MRI-guided single-nucleus RNA sequencing of chronic MS lesion edges.
  • Transcriptional profiling of glial and immune cells.
  • In vivo validation in mouse models (experimental autoimmune encephalomyelitis) and human MS tissue.

Main Results:

  • Identification of distinct glial phenotypes: 'microglia inflamed in MS' (MIMS) and 'astrocytes inflamed in MS'.
  • MIMS shares transcriptional profiles with microglia in other neurodegenerative diseases.
  • Complement component 1q (C1q) identified as a key mediator of MIMS activation.

Conclusions:

  • Shared mechanisms between MS and other neurodegenerative diseases suggest common therapeutic targets.
  • C1q inhibition presents a potential therapeutic strategy for chronic white matter inflammation in MS.
  • Paramagnetic rim lesions serve as a biomarker for monitoring therapeutic response to C1q blockade.