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Schizophrenia as a Disorder of Neurodevelopment
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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“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].”
From Prenatal nicotine exposure during pregnancy results in adverse neurodevelopmental alterations and neurobehavioral deficits (2023) · cites this paper as [102]
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Metadata
- Authors
- Lewis, D. A., & Levitt, P.
- Affiliations
- University of Pittsburgh (US)
- Venue
- Annual Review of Neuroscience
- Publisher
- Annual Reviews
- 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
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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