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CSMD1 regulates brain complement activity and circuit development.

Matthew L Baum1, Daniel K Wilton2, Rachel G Fox3

  • 1Department of Neurology, F.M. Kirby Neurobiology Center, Boston Children's Hospital, Harvard Medical School, Boston, MA 02115, USA; Department of Genetics, Harvard Medical School, Boston, MA 02115, USA; Stanley Center for Psychiatric Research, Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA; MD-PhD Program of Harvard & MIT, Harvard Medical School, Boston, MA 02115, USA.

Brain, Behavior, and Immunity
|March 29, 2024
PubMed
Summary
This summary is machine-generated.

CUB and Sushi Multiple Domains 1 (CSMD1) regulates complement-mediated synapse elimination in the developing brain. Loss of CSMD1 leads to increased complement deposition and altered neural circuit development, impacting brain health.

Keywords:
Complement cascadeComplement control proteinNeural circuitsSchizophreniaSynaptic pruning

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Area of Science:

  • Neuroscience
  • Immunology
  • Developmental Biology

Background:

  • Complement proteins are crucial for synaptic pruning during neurodevelopment.
  • Neural complement regulation remains poorly understood.
  • CUB and Sushi Multiple Domains 1 (CSMD1) regulates complement in vitro and is linked to schizophrenia risk.

Purpose of the Study:

  • To investigate the role of CSMD1 in regulating complement activity in the brain.
  • To examine CSMD1's involvement in complement-mediated synapse elimination during neurodevelopment.
  • To elucidate CSMD1's function in neural circuit development.

Main Methods:

  • Biochemical, immunohistochemical, and proteomic analyses of CSMD1 distribution and interactions in the brain.
  • Examination of Csmd1-knockout mice and CSMD1-knockout human neurons.
  • Analysis of synapse and circuit development in the mouse visual thalamus.
  • Quantification of complement deposition and microglial uptake of synaptosomes.

Main Results:

  • CSMD1 is localized at synapses and interacts with complement proteins in the brain.
  • Csmd1-knockout mice exhibit increased C3 deposition, reduced synapses, and aberrant visual circuit refinement.
  • Loss of CSMD1 enhances microglial engulfment of synaptosomes, dependent on CR3.
  • Human neurons lacking CSMD1 show increased vulnerability to complement deposition.

Conclusions:

  • CSMD1 acts as a regulator of complement-mediated synapse elimination in the developing brain.
  • Dysregulation of CSMD1 impacts synaptic refinement and neural circuit formation.
  • CSMD1 is a potential therapeutic target for neurodevelopmental disorders associated with complement dysregulation.