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Related Experiment Video

Updated: Jul 19, 2025

A Mouse Model for Vascular Cognitive Impairment and Dementia Based on Needle-guided Asymmetric Bilateral Common Carotid Artery Stenosis
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A Mouse Model for Vascular Cognitive Impairment and Dementia Based on Needle-guided Asymmetric Bilateral Common Carotid Artery Stenosis

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MCC950 ameliorates cognitive function by reducing white matter microstructure damage in rats after SAH.

Yunchuan Cao1, Yingwen Wang1, Xiaoguo Li1

  • 1Department of Neurosurgery, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China.

Brain Research Bulletin
|August 17, 2023
PubMed
Summary

MCC950, an inhibitor of the Nod-like receptor protein 3 (NLRP3) inflammasome, reduced white matter damage and improved cognitive function in rats following subarachnoid hemorrhage (SAH). This suggests a potential therapeutic strategy for cognitive impairment after SAH.

Keywords:
Cognitive functionMCC950NLRP3 inflammasomeSubarachnoid hemorrhageWhite matter microstructure

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Area of Science:

  • Neuroscience
  • Immunology

Background:

  • Subarachnoid hemorrhage (SAH) frequently causes cognitive impairment.
  • Neuroinflammation and white matter damage are key contributors to post-SAH cognitive deficits.
  • The Nod-like receptor protein 3 (NLRP3) inflammasome is implicated in SAH-induced neuroinflammation.

Purpose of the Study:

  • To investigate the therapeutic potential of MCC950, a specific NLRP3 inflammasome inhibitor, in a rat model of SAH.
  • To assess the effects of MCC950 on white matter microstructure and cognitive function after SAH.

Main Methods:

  • A subarachnoid hemorrhage (SAH) model was established in Sprague-Dawley rats via endovascular perforation.
  • MCC950 (10 mg/kg) was administered intraperitoneally one hour after SAH induction.
  • White matter microstructure integrity was evaluated, and behavioral tests were conducted to assess cognitive function.

Main Results:

  • MCC950 treatment significantly attenuated white matter microstructure damage in specific brain regions post-SAH.
  • Behavioral experiments demonstrated that MCC950 ameliorated cognitive deficits in rats subjected to SAH.
  • These findings highlight the role of NLRP3 inflammasome in SAH-induced white matter injury and cognitive impairment.

Conclusions:

  • Inhibition of the NLRP3 inflammasome with MCC950 shows a therapeutic effect on white matter microstructure damage and cognitive dysfunction following SAH.
  • MCC950 represents a potential therapeutic candidate for treating cognitive impairment in patients with subarachnoid hemorrhage.