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Related Experiment Videos

[Changes in glial cells in Binswanger-type infarction]

H Tomimoto1, I Akiguchi, H Wakita

  • 1Department of Neurology, Faculty of Medicine, Kyoto University, Japan.

No to Shinkei = Brain and Nerve
|August 1, 1994
PubMed
Summary

Glial cell activation, including microglia and astroglia, precedes white matter rarefaction in Binswanger-type infarction and chronic cerebral hypoperfusion models. This glial response may play a key role in the disease

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Cytopathological alterations and therapeutic approaches in Binswanger's disease.

Neuropathology : official journal of the Japanese Society of Neuropathology·2009

Area of Science:

  • Neuroscience
  • Pathology
  • Immunohistochemistry

Context:

  • Binswanger-type infarction is a form of cerebrovascular disease affecting white matter.
  • Chronic cerebral hypoperfusion is a condition of reduced blood flow to the brain.
  • Glial cells, including microglia, astroglia, and oligodendroglia, play crucial roles in brain health and disease.

Purpose:

  • To investigate immunohistochemical changes in glial cells in Binswanger-type infarction and chronic cerebral hypoperfusion.
  • To determine the role of glial cell activation in the pathogenesis of white matter rarefaction.

Summary:

  • Activated microglia (MHC class II antigen positive) and GFAP-immunoreactive astroglia were significantly increased in Binswanger-type infarction.
  • Chronic cerebral hypoperfusion in rats induced marked microglial activation and astroglial increase, persisting for 30 days.

Related Experiment Videos

  • A decrease in transferrin-immunoreactive oligodendroglia and white matter rarefaction were observed after 14 days of hypoperfusion.

    • Impact:

    • Findings suggest that chronic mild ischemia leads to white matter rarefaction.
    • Glial cell activation precedes white matter rarefaction and may be integral to the pathogenesis of Binswanger-type infarction.
    • This research provides insights into the cellular mechanisms underlying white matter damage in ischemic conditions.