Cited by 1,163Schizophrenia research and treatmentNeurotransmitter Receptor Influence on BehaviorAutism Spectrum Disorder Research

Schizophrenia as a Disorder of Neurodevelopment

Lewis, David A., Levitt, Pat·2002·Annual Review of Neuroscience

Abstract

▪ Abstract A combination of genetic susceptibility and environmental perturbations appear to be necessary for the expression of schizophrenia. In addition, the pathogenesis of the disease is hypothesized to be neurodevelopmental in nature based on reports of an excess of adverse events during the pre- and perinatal periods, the presence of cognitive and behavioral signs during childhood and adolescence, and the lack of evidence of a neurodegenerative process in most individuals with schizophrenia. Recent studies of neurodevelopmental mechanisms strongly suggest that no single gene or factor is responsible for driving a highly complex biological process. Together, these findings suggest that combinatorial genetic and environmental factors, which disturb a normal developmental course early in life, result in molecular and histogenic responses that cumulatively lead to different developmental trajectories and the clinical phenotype recognized as schizophrenia.

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Crossref · 10.1146/annurev.neuro.25.112701.142754

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  • Neurodevelopmental models of schizophrenia in animals typically involve exposure of the neonate during gestation or the perinatal period to adverse environmental insults such as maternal stress, hypoxia, malnutrition, or post-weaning social isolation that alter brain development and cause behavioral deficits into adulthood.

    “Neurodevelopmental models of schizophrenia in animals typically involve exposure of the neonate, either during gestation or the perinatal period, to adverse environmental insults such as maternal stress, hypoxia, malnutrition, or post-weaning social isolation that alter the brain development and cause behavioral deficits into adulthood [100–102].”

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Authors
Lewis, D. A., & Levitt, P.
Affiliations
University of Pittsburgh (US)
Venue
Annual Review of Neuroscience
Published
2002-03
Volume
25
Issue
1
Pages
409-432
ISSN
  • 0147-006X (ISSN-L)
  • 1545-4126
OpenAlex
W2112572641
Cited by
1,163
References
118
Citations by year
2026: 17 · 2025: 16 · 2024: 23 · 2023: 17 · 2022: 36 · 2021: 25 · 2020: 36 · 2019: 31 · 2018: 42 · 2017: 77 · 2016: 50 · 2015: 60 · 2014: 60 · 2013: 57 · 2012: 82
FWCI
7.83
Type
journal article
Language
en
Open access
closed
Locations
  • Annual Review of Neuroscience (publishedVersion)
  • PubMed (publishedVersion)
Funders
National Institute of Mental Health (MH 45156, P50MH045156)
Topics
  • Health Sciences › Medicine › Psychiatry and Mental health › Schizophrenia research and treatment
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
  • Life Sciences › Neuroscience › Cognitive Neuroscience › Autism Spectrum Disorder Research
Keywords
schizophrenia, brain development, genetic susceptibility, environmental risk factors, perinatal adversity, developmental trajectories, neurodegeneration, clinical phenotype
MeSH terms
Adolescent, Animals, Brain, Child, Developmental Disabilities, Child, Preschool, Female, Humans, Male, Models, Neurological, Nervous System Malformations, Pregnancy, Prenatal Exposure Delayed Effects, Schizophrenia, Gene Expression Regulation, Developmental, Genetic Predisposition to Disease

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