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A decrease of reelin expression as a putative vulnerability factor in schizophrenia

F Impagnatiello1, A R Guidotti, C Pesold

  • 1Psychiatric Institute, Department of Psychiatry, College of Medicine, University of Illinois, Chicago, IL 60612, USA.

Proceedings of the National Academy of Sciences of the United States of America
|December 23, 1998
PubMed
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Reelin (RELN) mRNA and protein are significantly reduced in schizophrenia patients across multiple brain regions. This suggests a neurodevelopmental basis for the disorder, potentially involving altered GABAergic signaling.

Area of Science:

  • Neuroscience
  • Molecular Psychiatry
  • Neurobiology

Background:

  • Schizophrenia is a complex psychiatric disorder with suspected neurodevelopmental origins.
  • Reelin (RELN) is a crucial extracellular matrix protein involved in neuronal migration and brain development.
  • Altered RELN signaling has been implicated in various neurological and psychiatric conditions.

Purpose of the Study:

  • To investigate reelin (RELN) mRNA and protein levels in postmortem brain tissues of schizophrenia patients.
  • To examine the expression of GABAergic and cholinergic receptor subunits to exclude postmortem artifacts.
  • To explore the relationship between RELN, its downstream targets, and the neurodevelopmental hypothesis of schizophrenia.

Main Methods:

  • Quantitative analysis of RELN mRNA and protein using postmortem prefrontal cortices, temporal cortices, hippocampi, caudate nuclei, and cerebella from schizophrenia patients and matched controls.

Related Experiment Videos

  • Measurement of gamma-aminobutyric acid (GABA)A receptor alpha1 and alpha5 subunit mRNAs, and nicotinic acetylcholine receptor alpha7 subunit mRNA.
  • Assessment of mouse disabled-1 (DAB1) protein and glutamate decarboxylase (GAD)65/67 protein levels.

    • Main Results:

    • Significant reduction (approx. 50%) in RELN mRNA and protein in all studied brain regions of schizophrenia patients.
    • Increased expression of GABAA receptor alpha1 and alpha5 subunits, while alpha7 nicotinic receptor subunit expression remained normal.
    • No significant changes in DAB1 protein levels, but a substantial decrease in GAD67 protein content was observed.

    Conclusions:

    • The findings support a significant deficit in reelin signaling in schizophrenia.
    • Altered GABAergic signaling, indicated by increased GABAA receptor subunits and decreased GAD67, may be linked to RELN dysfunction.
    • These results are consistent with a neurodevelopmental/vulnerability "two-hit" model for schizophrenia etiology.