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Related Experiment Video

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Preparation of Acute Hippocampal Slices from Rats and Transgenic Mice for the Study of Synaptic Alterations during Aging and Amyloid Pathology
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Hippocampal microglia CD40 mediates NPSLE cognitive dysfunction in mice.

Xiaoyue Qiao1, Hailin Wang1, Li Lu1

  • 1The State Key Laboratory of Pharmaceutical Biotechnology, Division of Immunology, Medical School, Nanjing University, Nanjing 210093, China.

Journal of Neuroimmunology
|June 1, 2021
PubMed
Summary

Neuropsychiatric lupus erythematosus (NPSLE) cognitive dysfunction involves microglia CD40 in the hippocampus. Inhibiting this protein improved brain damage and cognitive function in lupus mouse models.

Keywords:
Brain damageCD40Cognitive dysfunctionImiquimodMicrogliaNeuropsychiatric systemic lupus erythematosus

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Area of Science:

  • Neuroscience
  • Immunology
  • Pathology

Background:

  • Neuropsychiatric systemic lupus erythematosus (NPSLE) presents serious complications, with cognitive dysfunction being the most common symptom.
  • The precise mechanisms underlying NPSLE cognitive dysfunction are not fully understood, and the role of microglia CD40 has not been previously investigated.

Purpose of the Study:

  • To investigate the involvement of hippocampal microglia CD40 in cognitive dysfunction in MRL/MpJ-Faslpr (MRL/lpr) lupus mice.
  • To explore the potential of imiquimod (IMQ)-induced lupus mice as a model for NPSLE cognitive dysfunction.

Main Methods:

  • Quantitative polymerase chain reaction, western blotting, and immunohistochemistry were used to assess CD40 expression.
  • Flow cytometry and immunofluorescence identified the source of CD40.
  • Adeno-associated virus-mediated inhibition of microglia CD40 was employed.
  • Imiquimod (IMQ)-induced lupus mice were utilized.

Main Results:

  • Aberrant overexpression of hippocampal CD40 was observed in MRL/lpr lupus mice.
  • Overexpressed CD40 was primarily localized to hippocampal microglia.
  • Inhibition of microglia CD40 expression led to improvements in brain damage and cognitive dysfunction in MRL/lpr mice.
  • IMQ-induced lupus mice exhibited similar NPSLE cognitive dysfunction, brain damage, and hippocampal microglia CD40 overexpression as MRL/lpr mice.

Conclusions:

  • Hippocampal microglia CD40 plays a significant role in the pathogenesis of NPSLE cognitive dysfunction.
  • IMQ-induced lupus mice represent a novel and relevant model for studying NPSLE cognitive dysfunction.
  • Targeting microglia CD40 offers a potential therapeutic strategy for NPSLE-associated cognitive impairment.