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Deleting the complement protein C1q in Alzheimer's disease (AD) mouse models rescues synaptic density regardless of deletion timing. This study investigates C1q's role in neuroinflammation and amyloid clearance in AD.

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Area of Science:

  • Neuroscience
  • Immunology

Background:

  • The complement system, particularly C1q, exacerbates neuroinflammation and cognitive decline in Alzheimer's disease (AD).
  • Previous research indicates that constitutive C1q deletion mitigates glial activation and neuronal loss in AD models.

Purpose of the Study:

  • To investigate the impact of global C1q deletion at different disease stages on neuroinflammation, synaptic loss, and amyloid phagocytosis in an AD mouse model.

Main Methods:

  • Arctic AD mice with inducible C1q deletion (C1qaFL/FLRosaCreERT2) were treated with tamoxifen at 11 or 20 weeks.
  • Neuroinflammation was assessed via C3, GFAP, C5aR1, and Iba1 staining.
  • Synaptic density was evaluated using superresolution microscopy (Vglut1-Psd95).
  • Amyloid phagocytosis by microglia was quantified via confocal microscopy.

Main Results:

  • Late C1q deletion (20 weeks) significantly reduced microglial (Iba1) and C3 expression.
  • Early C1q deletion (11 weeks) significantly reduced C3 expression.
  • Global C1q deletion at both 11 and 20 weeks rescued synaptic density (Vglut1-Psd95) in the CA3 region.
  • Microglial-amyloid colocalization increased with early C1q deletion, but phagocytosis remained unchanged.

Conclusions:

  • Global C1q deletion rescues synaptic density in the Arctic AD mouse model, irrespective of the deletion timing.
  • C1q deletion reduces specific markers of neuroinflammation (C3, GFAP) and microglial activation, particularly when induced later in the disease.
  • The rescue of synaptic density is independent of altered amyloid phagocytosis by microglia.