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Cortical development and neuropathology in schizophrenia
1Department of Anatomy and Neurobiology, University of California, Irvine 92717, USA.
Ciba Foundation Symposium
|January 1, 1995
Summary
Pregnancy disruptions may increase schizophrenia risk. Impaired fetal brain development, specifically in neuronal migration and cortical connections, is hypothesized to underlie schizophrenia development.
Area of Science:
- Neuroscience
- Developmental Neuroscience
- Psychiatry
Background:
- Epidemiological studies link prenatal exposures to increased schizophrenia incidence.
- Neuropathological findings in schizophrenia suggest defects in late-stage cerebral cortical development, including neuronal migration and connection patterning.
- The precise relationship between early brain lesions and later circuitry dysfunction in schizophrenia remains unclear.
Purpose of the Study:
- To propose a hypothesis for the neuropathological basis of schizophrenia.
- To investigate the role of subplate zone disturbances in cortical development and schizophrenia.
- To link early developmental defects to later functional and molecular alterations in schizophrenia.
Main Methods:
- Neuromorphological studies.
- Gene expression analysis.
- Hypothesis formulation based on existing data.
Main Results:
- A disturbance in neuronal migration or programmed cell death in the subplate zone is hypothesized.
- This disturbance leads to aberrant cortical circuitry formation.
- Compromised circuitry may result in schizophrenic symptoms and altered neurotransmitter/receptor gene expression.
Conclusions:
- Prenatal insults affecting subplate development may initiate a cascade leading to schizophrenia.
- Failure to establish normal cortical connections is a potential key mechanism.
- Activity-dependent gene expression changes reflect downstream consequences of this developmental defect.