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CX3C-chemokine receptor 1 modulates cognitive dysfunction induced by sleep deprivation

Jiawei Xin1,2,3, Chao Wang1,2,3, Xiaojuan Cheng1,2,3

  • 1Department of Neurology, Fujian Institute of Geriatrics, Fujian Medical University Union Hospital, Fuzhou, Fujian 350001, China.

Chinese Medical Journal
|November 4, 2021
PubMed
Abstract

Insights

CX3C-chemokine receptor 1 (CX3CR1) deficiency in microglia prevents cognitive decline from sleep deprivation by reducing neuroinflammation and altering synaptic pruning. This suggests CX3CR1 is a potential therapeutic target for sleep loss-related cognitive impairment.

Area of Science:

  • Neuroscience
  • Immunology
  • Sleep Research

Background:

  • Microglia are crucial in sleep deprivation (SD) pathology.
  • CX3C-chemokine receptor 1 (CX3CR1) on microglia may influence cognitive decline during SD.
  • Investigating CX3CR1 knockout effects on the central nervous system's response to SD is key.

Purpose of the Study:

  • To evaluate the role of microglial CX3CR1 in cognitive decline associated with sleep deprivation.
  • To understand how CX3CR1 deficiency impacts neuroinflammation and synaptic pruning during SD.
  • To determine if interfering with microglial function via CX3CR1 knockout affects the CNS response to SD.

Main Methods:

  • Middle-aged wild-type and CX3CR1 knockout mice were subjected to 8 hours of sleep deprivation (SD) or normal sleep (S).
  • Behavioral and histological tests were employed to assess changes.
  • Mice models mimicked pathophysiological changes in middle-aged individuals after staying up all night.

Main Results:

  • CX3CR1 deficiency protected against SD-induced cognitive impairments.
  • CX3CR1 knockout mice showed reduced microglia and c-Fos density in the dentate gyrus (DG) post-SD.
  • Reduced pro-inflammatory cytokines and microglial phagocytosis, alongside increased anti-inflammatory cytokines and DG spine density, were observed in CX3CR1-/- SD mice.

Conclusions:

  • CX3CR1 deficiency alters cerebral responses to sleep deprivation.
  • Reduced neuroinflammation and modified synaptic pruning are potential mechanisms.
  • CX3CR1 emerges as a potential therapeutic target for preventing sleep loss-induced cognitive impairments.

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