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Related Experiment Videos

Decrease in reelin and glutamic acid decarboxylase67 (GAD67) expression in schizophrenia and bipolar disorder: a

A Guidotti1, J Auta, J M Davis

  • 1Psychiatric Institute, University of Illinois at Chicago, 1601 W Taylor St, Room 256, Chicago, IL 60612, USA. aguidotti@psych.uic.edu

Archives of General Psychiatry
|November 14, 2000
PubMed
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This summary is machine-generated.

Reelin (RELN) and glutamic acid decarboxylase (GAD)67 are reduced in the brains of patients with schizophrenia and bipolar disorder with psychosis. These changes may indicate vulnerability factors for psychosis.

Area of Science:

  • Neuroscience
  • Psychiatry
  • Molecular Biology

Background:

  • Reelin (RELN) is a glycoprotein crucial for neuronal development, primarily secreted by GABAergic interneurons.
  • RELN interacts with disabled-1 (DAB1) to mediate its signaling pathway.
  • Previous studies indicated reduced RELN and GAD(67) in schizophrenia, but not DAB1.

Purpose of the Study:

  • To replicate findings of down-regulated RELN and GAD(67) in schizophrenia.
  • To investigate if these deficits extend to other psychiatric disorders like bipolar disorder and unipolar depression.
  • To analyze the expression of RELN, GAD(65), GAD(67), DAB1, and neuron-specific-enolase in postmortem brains.

Main Methods:

  • Quantitative reverse transcriptase-polymerase chain reaction (RT-PCR) and Western blot analyses were used to measure mRNA and protein levels.

Related Experiment Videos

  • Immunohistochemistry identified Reelin-positive neurons.
  • A cohort of 60 postmortem brains, including patients with schizophrenia, bipolar disorder, unipolar depression, and nonpsychiatric controls, was analyzed.

    • Main Results:

    • Significant decreases (30-50%) in prefrontal cortex RELN mRNA, GAD(67) protein/mRNA, and RELN-positive cells were observed in patients with schizophrenia or bipolar disorder with psychosis.
    • No significant differences in DAB1, GAD(65), or neuron-specific-enolase expression were found, suggesting the down-regulations are not due to general neuronal damage.
    • RELN and GAD(67) down-regulations were independent of postmortem intervals and antipsychotic medication.

    Conclusions:

    • Selective down-regulation of RELN and GAD(67) in the prefrontal cortex of patients with psychosis (schizophrenia, bipolar disorder) supports their role as vulnerability factors.
    • The loss of correlation between RELN and GAD(67) in psychotic patients, compared to nonpsychotic individuals, suggests these changes are liability factors for psychosis.