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Related Concept Videos

Biological Causes of Schizophrenia01:29

Biological Causes of Schizophrenia

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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.
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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.
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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.
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Genome-wide association studies or GWAS are used to identify whether common SNPs are associated with certain diseases. Suppose specific SNPs are more frequently observed in individuals with a particular disease than those without the disease. In that case, those SNPs are said to be associated with the disease. Chi-square analysis is performed to check the probability of the allele likely to be associated with the disease.
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Gene expression analysis of Schizophrenia.

Gunjan Sharma1, Ansh Malik1, Satyendra Tripathi2,3

  • 1AIIMS Nagpur, India.

Bioinformation
|March 31, 2025
PubMed
Summary

Schizophrenia involves prefrontal cortex gray matter loss. Gene expression analysis revealed immune dysfunction and apoptosis linked to upregulated genes, and suppressed EGF pathways linked to downregulated genes, offering potential therapeutic targets.

Keywords:
BiomarkersDysfunctional immunityGene expressionPrefrontal cortexSchizophrenia

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Area of Science:

  • Neuroscience
  • Genetics
  • Psychiatry

Background:

  • Schizophrenia is a chronic psychiatric disorder characterized by cognitive deficits.
  • Prefrontal cortical dysfunction, specifically in Broadmann Area 10 (BA 10), is implicated, with observed gray matter reduction.
  • The underlying genetic mechanisms contributing to these abnormalities are not well understood.

Purpose of the Study:

  • To investigate altered gene expression and associated pathways in the prefrontal cortex of schizophrenia patients.
  • To identify potential genetic biomarkers and therapeutic targets for schizophrenia.

Main Methods:

  • Utilized two Gene Expression Omnibus (GEO) datasets: GSE12654 (discovery) and GSE17612 (validation).
  • Performed differential gene expression analysis between schizophrenia patients and healthy controls.
  • Conducted protein-protein interaction analysis to understand pathway associations.

Main Results:

  • Validated three upregulated genes (S100A9, S100A8, BCL2A1) and one downregulated gene (CBLB).
  • Upregulated genes were associated with immune response and apoptotic processes.
  • Downregulated genes were linked to the suppression of Epidermal Growth Factor (EGF) pathways.

Conclusions:

  • Findings suggest a role for immune dysfunction and apoptotic processes in schizophrenia pathophysiology.
  • The identified gene expression changes correlate with gray matter loss observed in the prefrontal cortex.
  • The study highlights S100A9, S100A8, BCL2A1, and CBLB as potential biomarkers and therapeutic targets for schizophrenia.