The DOI matches its Crossref record; 118 of the 118 references it cites were found in a registry or an index.
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]
Citations
Cites
Implications of Normal Brain Development for the Pathogenesis of Schizophrenia
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The Molecular Biology of Axon Guidance
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Synaptic density in human frontal cortex —Developmental changes and effects of aging
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A review of MRI findings in schizophrenia
Shenton, M. E., Dickey, C. C., Frumin, M., & McCarley, R. W. (2001) · Schizophrenia Research · doi:10.1016/s0920-9964(01)00163-3 · Cited by 2,346
Neuronal specification in the spinal cord: inductive signals and transcriptional codes
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Decreased apoptosis in the brain and premature lethality in CPP32-deficient mice
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Risch, N. J. (2000) · Nature · doi:10.1038/35015718 · Cited by 1,839
Schizophrenia: Caused by a fault in programmed synaptic elimination during adolescence?
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Research works printed but not linked: 3
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Cited by
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The Endophenotype Concept in Psychiatry: Etymology and Strategic Intentions
Gottesman, I. I., & Gould, T. D. (2003) · American Journal of Psychiatry · doi:10.1176/appi.ajp.160.4.636 · Cited by 5,615
Schizophrenia as a Complex Trait: Evidence From a Meta-analysis of Twin Studies
Sullivan, P. F., Kendler, K. S., & Neale, M. C. (2003) · Archives of General Psychiatry · doi:10.1001/archpsyc.60.12.1187 · Cited by 2,356
Synaptic Plasticity: Multiple Forms, Functions, and Mechanisms
Citri, A., & Malenka, R. C. (2008) · Neuropsychopharmacology · doi:10.1038/sj.npp.1301559 · Cited by 2,323
Cortical inhibitory neurons and schizophrenia
Lewis, D. A., Hashimoto, T., & Volk, D. W. (2005) · Nature Reviews Neuroscience · doi:10.1038/nrn1648 · Cited by 2,297
Self-citationAbnormal neural oscillations and synchrony in schizophrenia
Uhlhaas, P. J., & Singer, W. (2010) · Nature Reviews Neuroscience · doi:10.1038/nrn2774 · Cited by 2,120
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
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