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COG1410 Alleviated Chronic Sleep Deprivation-Induced Memory Loss by Regulating Microglial Phagocytosis and Inhibiting

Peng Wu1, Chao Fu1,2, Min Chen3

  • 1Department of Anesthesiology, Jinan University First Affiliated Hospital, 613# The West of Huangpu Avenue, Tianhe District, Guangzhou 510630, Guangdong, China.

ACS Chemical Neuroscience
|July 9, 2025
PubMed

Insights

Sleep deprivation impairs memory consolidation by increasing microglial synapse removal. The peptide COG1410 partially rescues this impairment by modulating microglial activity and reducing inflammation.

Area of Science:

  • Neuroscience
  • Sleep Research
  • Neuroimmunology

Background:

  • Sleep loss negatively impacts cognitive functions in adults.
  • Microglia play a role in synaptic pruning during sleep, essential for memory consolidation.

Purpose of the Study:

  • To investigate the effects of sleep deprivation on synaptic plasticity and memory in mice.
  • To evaluate the potential of the APOE mimic peptide COG1410 in mitigating sleep deprivation-induced memory deficits.

Main Methods:

  • Established a sleep deprivation mouse model using the modified multiple-platform method (MMPM).
  • Utilized western blotting, immunofluorescence, and Golgi-Cox staining to assess synaptic changes and microglial activity.
  • Administered COG1410 and employed small interfering RNA (siRNA) to downregulate TREM2 expression.

Main Results:

  • Sleep deprivation increased microglial phagocytosis of mature synapses, reducing their number and impairing long-term memory consolidation.
  • COG1410 pretreatment partially restored long-term memory, alleviated abnormal microglial phagocytosis, and increased mature synapses.
  • COG1410 promoted M2 microglial polarization and reduced hippocampal inflammation; TREM2 downregulation diminished COG1410's protective effects.

Conclusions:

  • Sleep deprivation-induced memory impairment is linked to excessive microglial phagocytosis of synapses.
  • COG1410 demonstrates potential therapeutic value by preserving synaptic integrity and reducing neuroinflammation.
  • The protective mechanism of COG1410 involves TREM2-dependent modulation of microglial function.
Keywords:
COG1410chronic sleep deprivationhippocampusmemory lossmicrogliaphagocytosis

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