Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Psychosis: Pathophysiology of Schizophrenia and Other Psychotic Disorders

Psychosis: Pathophysiology of Schizophrenia and Other Psychotic Disorders

Schizophrenia is a neurodevelopmental disorder whose origins are rooted in complex genetic components. Despite our burgeoning understanding, the pathophysiology of this disorder remains incompletely deciphered.
Researchers have identified genetic factors that increase susceptibility to schizophrenia, underscoring the intricate interplay between genetics and environment in disease development. At the core of schizophrenia's pathophysiology is excessive dopaminergic neurotransmission within...

Complement System

Complement System

The complement system is a group of approximately 20 plasma proteins that strengthen the body's defenses against infections through opsonization, inflammation, and cell lysis. Opsonization involves coating pathogens with complement proteins, making them more recognizable and facilitating phagocyte engulfment. Certain complement proteins induce inflammation that attracts immune cells to the site of infection. Cell lysis involves the destruction of pathogens through the formation of a...

Biological Causes of Schizophrenia

Biological Causes of Schizophrenia

Schizophrenia, a severe psychiatric disorder, arises from a complex interplay of biological factors, including genetic predisposition, structural brain abnormalities, neurotransmitter dysregulation, and developmental irregularities. These factors collectively contribute to the onset and progression of the disorder, which typically manifests in late adolescence or early adulthood.
Genetic Factors in Schizophrenia
The genetic basis of schizophrenia is strongly supported by family and twin...

Psychological and Sociocultural Causes of Schizophrenia

Psychological and Sociocultural Causes of Schizophrenia

Schizophrenia, a complex psychiatric disorder, has been historically misunderstood. Early psychological theories attributed its origins to childhood trauma and unresponsive parenting. However, contemporary research largely rejects these notions, favoring the vulnerability-stress hypothesis. This model proposes that individuals with a genetic predisposition to schizophrenia may develop the disorder following exposure to significant environmental stressors. Notably, studies on high-risk...

Human Genetics

Human Genetics

Human genetics provides a profound framework for understanding the interplay between genetic predispositions and human psychology. At the heart of this discipline lies the study of how genes influence physical traits, behaviors, and susceptibility to diseases. Each person carries a unique genetic code that subtly or significantly shapes their psychological and behavioral landscape.
The complex relationship between genetics and psychology is observable through common biological components such...

Gene-Environment Interactions

Gene-Environment Interactions

Gene expression is a dynamic process that is significantly influenced by environmental factors. This interaction underlies the complex nature of biological development and the phenotypic differences observed among individuals, even among those with identical genetic makeups. Factors such as radiation, temperature, behavior, nutrition, and stress play pivotal roles in determining how genes are expressed. The concept of the reaction range is central to understanding this interaction. It posits...

You might also read

Related Articles

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

Sort by

Same author

Valacyclovir Treatment of Early Symptomatic Alzheimer Disease: The VALAD Randomized Clinical Trial.

JAMA·2025

Same author

Toxoplasma gondii, Herpesviridae and long-term risk of transition to first-episode psychosis in an ultra high-risk sample.

Schizophrenia research·2021

Same author

Heritable anisotropy associated with cognitive impairments among patients with schizophrenia and their non-psychotic relatives in multiplex families.

Psychological medicine·2020

Same author

Antiviral therapy: Valacyclovir Treatment of Alzheimer's Disease (VALAD) Trial: protocol for a randomised, double-blind,placebo-controlled, treatment trial.

BMJ open·2020

Same author

Multiple rare inherited variants in a four generation schizophrenia family offer leads for complex mode of disease inheritance.

Schizophrenia research·2019

Same author

Rare variant based evidence for oligogenic contribution of neurodevelopmental pathway genes to schizophrenia.

Schizophrenia research·2019

Search research articles

Related Experiment Video

Updated: Feb 25, 2026

Derivation, Expansion, Cryopreservation and Characterization of Brain Microvascular Endothelial Cells from Human Induced Pluripotent Stem Cells

Derivation, Expansion, Cryopreservation and Characterization of Brain Microvascular Endothelial Cells from Human Induced Pluripotent Stem Cells

Published on: November 19, 2020

The complement system: a gateway to gene-environment interactions in schizophrenia pathogenesis.

V L Nimgaonkar^1,2, K M Prasad¹, K V Chowdari¹

¹Department of Psychiatry, University of Pittsburgh, School of Medicine, Pittsburgh, PA, USA.

Molecular Psychiatry

|August 2, 2017

Summary

Schizophrenia pathogenesis may involve gene-environment interactions (GEI) and a dysregulated complement system. Recent studies link complement C4A/C4B gene variations to schizophrenia risk, suggesting new research directions.

More Related Videos

Gene-environment Interaction Models to Unmask Susceptibility Mechanisms in Parkinson's Disease

Gene-environment Interaction Models to Unmask Susceptibility Mechanisms in Parkinson's Disease

Published on: January 7, 2014

High-resolution Melting PCR for Complement Receptor 1 Length Polymorphism Genotyping: An Innovative Tool for Alzheimer's Disease Gene Susceptibility Assessment

High-resolution Melting PCR for Complement Receptor 1 Length Polymorphism Genotyping: An Innovative Tool for Alzheimer's Disease Gene Susceptibility Assessment

Published on: July 18, 2017

Related Experiment Videos

Last Updated: Feb 25, 2026

Derivation, Expansion, Cryopreservation and Characterization of Brain Microvascular Endothelial Cells from Human Induced Pluripotent Stem Cells

Derivation, Expansion, Cryopreservation and Characterization of Brain Microvascular Endothelial Cells from Human Induced Pluripotent Stem Cells

Published on: November 19, 2020

Gene-environment Interaction Models to Unmask Susceptibility Mechanisms in Parkinson's Disease

Gene-environment Interaction Models to Unmask Susceptibility Mechanisms in Parkinson's Disease

Published on: January 7, 2014

High-resolution Melting PCR for Complement Receptor 1 Length Polymorphism Genotyping: An Innovative Tool for Alzheimer's Disease Gene Susceptibility Assessment

High-resolution Melting PCR for Complement Receptor 1 Length Polymorphism Genotyping: An Innovative Tool for Alzheimer's Disease Gene Susceptibility Assessment

Published on: July 18, 2017

Area of Science:

Neuroscience
Immunology
Genetics

Background:

Schizophrenia pathogenesis is complex, involving multiple factors and gene-environment interactions (GEI).
Growing evidence implicates the complement system, a key immune pathway, in schizophrenia.
Previous studies showed inconclusive results regarding complement activity in schizophrenia.

Purpose of the Study:

To explore the role of the complement system in schizophrenia pathogenesis.
To investigate gene-environment interactions (GEI) related to complement genes and schizophrenia risk.
To identify new therapeutic avenues by understanding the complement system's involvement.

Main Methods:

Review of existing literature on schizophrenia, complement pathways, and genetic studies.
Analysis of genome-wide association studies (GWAS) identifying complement 4A (C4A) and 4B (C4B) gene polymorphisms.
Exploration of rodent models demonstrating complement's role in neurodevelopment and synaptic pruning.

Main Results:

Recent GWAS highlight C4A/C4B gene repeat polymorphisms as significant risk factors for schizophrenia.
Complement system dysregulation is increasingly recognized as a pathogenic process in schizophrenia.
Complement proteins are implicated in neurodevelopmental processes like synaptic pruning.

Conclusions:

The complement system offers a promising framework for studying schizophrenia pathogenesis, particularly GEI.
Further research on C4A/C4B polymorphisms and their interaction with environmental factors is warranted.
Understanding complement pathways may lead to novel therapeutic strategies for schizophrenia.