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A Versatile Murine Model of Subcortical White Matter Stroke for the Study of Axonal Degeneration and White Matter Neurobiology
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Axonal abnormalities in vanishing white matter.

Melanie D Klok1, Marianna Bugiani2, Sharon I de Vries3

  • 1Department of Pediatrics/Child Neurology Amsterdam Neuroscience VU University Medical Centre Amsterdam The Netherlands.

Annals of Clinical and Translational Neurology
|April 25, 2018
PubMed
Summary
This summary is machine-generated.

In vanishing white matter, axons initially develop normally but later atrophy. Astrocytes play a key role in this axonal pathology, suggesting early intervention could prevent damage.

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Area of Science:

  • Neuroscience
  • Cell Biology
  • Genetics

Background:

  • Vanishing white matter (VWM) is a severe leukodystrophy.
  • The precise mechanisms of axonal pathology and the role of glial cells in VWM remain incompletely understood.

Purpose of the Study:

  • To investigate the temporal development of axonal and myelin pathology in VWM.
  • To elucidate the contribution of astrocytes to axonal damage in VWM.

Main Methods:

  • Analysis of axons and myelin using electron microscopy and immunohistochemistry in Eif2b4 and Eif2b5 mutant mice and human VWM brain tissue.
  • In vitro astrocyte-forebrain co-culture experiments.

Main Results:

  • Mutant mice showed normal early development of axons and myelin, followed by axonal thinning and increased axonal density.
  • Mutant astrocytes induced axonal pathology in co-cultures, while control astrocytes did not.
  • VWM patient brains exhibited thinner axons and myelin sheaths in affected white matter areas.

Conclusions:

  • Axonal pathology in VWM is a progressive process involving later-stage atrophy.
  • Astrocytes are critical mediators of axonal damage in VWM.
  • Early therapeutic intervention may prevent irreversible axonal damage in VWM.