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Published on: March 2, 2018
The neurodevelopmental hypothesis of schizophrenia: convergent clues from epidemiology and neuropathology
Michael Piper1, Monica Beneyto, Thomas H J Burne
1School of Biomedical Science, University of Queensland, St Lucia, Queensland 4072, Australia.
Insights
Schizophrenia risk is linked to early brain development disruptions. Evidence from epidemiology, genetics, neuropathology, and animal models supports this neurodevelopmental hypothesis.
Area of Science:
- Neuroscience
- Psychiatry
- Developmental Biology
Background:
- The neurodevelopmental hypothesis of schizophrenia posits that early brain development disruptions elevate schizophrenia risk.
- This theory highlights critical developmental periods and associated risk factors.
Purpose of the Study:
- To review evidence supporting the neurodevelopmental hypothesis of schizophrenia.
- To integrate findings from epidemiology, genetics, neuropathology, and animal models.
Main Methods:
- Epidemiological studies identifying prenatal/perinatal risk factors (infection, nutrition, obstetric complications).
- Genetic studies examining candidate genes associated with brain development.
- Neuropathological research investigating brain abnormalities.
- Animal models exploring effects of early life exposures on brain systems.
Main Results:
- Epidemiological data links various prenatal and perinatal factors to schizophrenia.
- Genetic research implicates specific genes in altered brain development.
- Neuropathological findings corroborate early developmental disruptions.
- Animal models demonstrate that early life exposures impact relevant brain systems.
Conclusions:
- Convergent evidence from multiple disciplines supports the neurodevelopmental hypothesis of schizophrenia.
- Disruptions in early brain development are strongly implicated in schizophrenia pathogenesis.
Abstract:
The neurodevelopmental hypothesis of schizophrenia suggests that the disruption of early brain development increases the risk of later developing schizophrenia. This hypothesis focuses attention on critical periods of early brain development. From an epidemiologic perspective, various prenatal and perinatal risk factors have been linked to schizophrenia, including exposures related to infection, nutrition, and obstetric complications. From a genetic perspective, candidate genes have also been linked to altered brain development. In recent decades evidence from neuropathology has provided support for the neurodevelopmental hypothesis. Animal models involving early life exposures have been linked to changes in these same brain systems, providing convergent evidence for this long-standing hypothesis.
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