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Microglial TLR4 is Critical for Neuronal Injury and Cognitive Dysfunction in Subarachnoid Hemorrhage.

Rezwanul Islam1, Frank Vrionis1,2, Khalid A Hanafy3,4

  • 1Department of Biomedical Sciences, Charles E. Schmidt College of Medicine, Florida Atlantic University, Boca Raton, FL, USA.

Neurocritical Care
|July 1, 2022
PubMed
Summary

Microglial Toll-like receptor 4 (TLR4) activation drives neuroinflammation and cognitive decline after subarachnoid hemorrhage (SAH). Targeting microglial TLR4 offers a promising therapeutic strategy for SAH-induced brain injury and cognitive dysfunction.

Keywords:
Cognitive dysfunctionMicrogliaNeuronal injurySubarachnoid hemorrhageToll-like receptor

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Area of Science:

  • Neuroscience
  • Immunology
  • Pathology

Background:

  • Toll-like receptor 4 (TLR4) activation promotes neuroinflammation in subarachnoid hemorrhage (SAH) by increasing proinflammatory mediators and costimulatory molecules.
  • The specific glial cells involved in initiating and propagating SAH-induced neuroinflammation remain unclear.

Purpose of the Study:

  • To investigate the role of glial TLR4, specifically in microglia and astrocytes, in SAH-related brain damage and neurological outcomes.
  • To determine if targeting microglial TLR4 can mitigate SAH-induced neuroinflammation and cognitive deficits.

Main Methods:

  • Utilized global and cell-specific TLR4 knockout mice, including microglia-specific and astrocyte/neuron-specific knockouts, alongside wildtype controls.
  • Induced SAH by injecting autologous blood and assessed outcomes on postoperative day 7 via immunohistochemistry, microglial morphology analysis, and Barnes maze for cognitive function.
  • Investigated the effect of microglial depletion using clodronate liposomes on neuronal apoptosis and cognitive performance.

Main Results:

  • Microglial depletion significantly reduced neuronal apoptosis and improved cognitive performance in the SAH mouse model.
  • TLR4 knockout in microglia, but not in astrocytes or neurons, significantly reduced microglial activation, neuronal apoptosis, and improved cognitive outcomes compared to wildtype.
  • Mice lacking TLR4 on astrocytes and neurons showed no significant differences compared to wildtype mice.

Conclusions:

  • Microglial TLR4 is critical for mediating microglial activation, neuronal injury, and cognitive dysfunction following SAH.
  • Targeting microglial TLR4 presents a potential therapeutic avenue for treating SAH-associated brain damage and cognitive impairment.
  • Microglial depletion strategies, such as clodronate administration, can ameliorate cognitive deficits in SAH models.