Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Schizophrenia: Complement Cleaning or Killing.

Jirrine T T Hogenaar1, Hans van Bokhoven1,2

  • 1Donders Institute for Brain, Cognition and Behaviour, Radboud university medical center, P.O. Box 9101, 6500 HB Nijmegen, The Netherlands.

Genes
|March 6, 2021
PubMed
Summary
This summary is machine-generated.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Astrocytes contribute to olanzapine-mediated reversal of Kleefstra Syndrome-associated neurodevelopmental regression.

The Journal of clinical investigation·2026
Same author

Generation of isogenic rescue iPSC lines by targeted CTG-repeat excision for myotonic dystrophy type 1.

Stem cell research·2026
Same author

Biallelic rescue of CTG18.1 in two Fuchs endothelial corneal dystrophy-derived iPSC lines (SCTCi047-A-2, SCTCi046-A-2) following a two-step gene editing strategy.

Stem cell research·2026
Same author

Generation of iPSC lines from myotonic dystrophy type 1 patients with varying CTG repeat lengths.

Stem cell research·2026
Same author

Human neuronal networks on micro-electrode arrays as a tool to assess genotype-phenotype correlation in CACNA1A-related disorders.

Stem cell reports·2026
Same author

Biallelic excision of the CTG18.1 expansion in two Fuchs endothelial corneal dystrophy-derived iPSC lines and one control (SCTCi046-A-1, SCTCi047-A-1 and SCTCi041-A-1) using an episomal vector-based CRISPR/Cas9 approach.

Stem cell research·2025
Same journal

Tissue MicroRNAs in Arrhythmogenic Cardiomyopathy: A Systematic Review of Studies in Human Myocardium and Animal Models with Implications for Post-Mortem Molecular Diagnostics.

Genes·2026
Same journal

Genetic Variants and Dental Caries Susceptibility: An Umbrella Review and Multilevel Meta-Analysis.

Genes·2026
Same journal

Generative AI and Language Models in Human Genetics and Health: From Variant Interpretation to Clinical Decision Support.

Genes·2026
Same journal

Familial White-Sutton Syndrome Caused by a Pathogenic POGZ p.Arg508* Variant: Intrafamilial Variability from Childhood to Adulthood.

Genes·2026
Same journal

Genetic Influence on LDL-Cholesterol Levels: Role of Polygenic Risk Scores and Lp(a) Beyond Monogenic Hypercholesterolemia.

Genes·2026
Same journal

THBS1 as a Key Regulator of Myoblasts: Validation of Its Inhibitory Roles in Skeletal Muscle Development.

Genes·2026
See all related articles

The classical complement pathway may excessively prune synapses in schizophrenia, contributing to cognitive deficits. Further research is needed to understand this mechanism and develop targeted therapies.

Area of Science:

  • Neuroscience
  • Immunology
  • Psychiatry

Background:

  • Schizophrenia is a complex psychiatric disorder with onset typically in adolescence or young adulthood.
  • Reduced cortical synaptic density in schizophrenia suggests excessive synaptic elimination.
  • The complement system is implicated in synaptic pruning during development.

Purpose of the Study:

  • To review genetic and functional evidence for the classical complement pathway's role in schizophrenia.
  • To consider the impact of complement protein deficiencies.
  • To evaluate the complement system's contribution to synaptic pruning and cognitive impairment.

Main Methods:

  • Review of genetic and functional studies on classical complement pathway components.
  • Analysis of human complement protein deficiency data.
Keywords:
complement systemschizophreniasynaptic pruning

Related Experiment Videos

  • Synthesis of evidence linking complement activity to synaptic elimination.
  • Main Results:

    • Strong evidence suggests the classical complement pathway contributes to excessive synaptic pruning in schizophrenia.
    • Complement protein deficiencies offer insights into pathway function.
    • This overactivity is linked to cognitive impairment in schizophrenia patients.

    Conclusions:

    • The classical complement pathway is a significant factor in excessive synaptic pruning in schizophrenia.
    • Understanding complement-mediated pruning mechanisms is crucial for developing targeted schizophrenia treatments.
    • Future studies should quantify complement's contribution to schizophrenia phenotypes and elucidate pruning mechanisms.