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Complement C1q-C3-associated synaptic changes in multiple sclerosis hippocampus.

Iliana Michailidou1, Janske G P Willems1,2, Evert-Jan Kooi3

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Summary
This summary is machine-generated.

The complement system, specifically C1q and C3, is implicated in synaptic loss in multiple sclerosis (MS) brains. This suggests a novel therapeutic target for MS-related memory impairment.

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Area of Science:

  • Neuroimmunology
  • Neurodegeneration
  • Complement System Biology

Background:

  • Multiple Sclerosis (MS) is a central nervous system demyelinating disease.
  • Memory impairment affects up to 65% of MS patients, linked to hippocampal synaptic loss.
  • The molecular mechanisms underlying synaptic loss in MS remain unclear.

Purpose of the Study:

  • To investigate the role of the complement system, specifically C1q and C3, in synaptic alterations within the MS hippocampus.
  • To analyze the relationship between complement components, synaptic density, and neuropathological markers in MS brains.

Main Methods:

  • Gene and protein expression and localization of C1q and C3 were analyzed in postmortem MS hippocampi.
  • Neuropathological changes, synaptic density, and neuronal stress markers (mtHSP70) were assessed.
  • Comparisons were made with Alzheimer disease (AD) and non-neurological control hippocampi.

Main Results:

  • Increased C1q and C3 activation were observed in MS hippocampi, particularly in CA3/2 and CA1 subfields.
  • MS hippocampi showed reduced synaptic density and increased neuronal mtHSP70, correlating with C1q density.
  • C1q and C3 localized at synapses, suggesting microglial engulfment of complement-tagged synapses; MS brains lacked C5b9.

Conclusions:

  • The C1q-C3 complement axis plays a significant role in synaptic alterations in the MS hippocampus.
  • These findings highlight a potential molecular pathway contributing to memory dysfunction in MS.