Cited by 860Schizophrenia research and treatmentTryptophan and brain disordersMental Health and Psychiatry

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The Neurodevelopmental Hypothesis of Schizophrenia, Revisited

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Fatemi, S. H., Folsom, T. D.·2009·Schizophrenia Bulletin

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Abstract

While multiple theories have been put forth regarding the origin of schizophrenia, by far the vast majority of evidence points to the neurodevelopmental model in which developmental insults as early as late first or early second trimester lead to the activation of pathologic neural circuits during adolescence or young adulthood leading to the emergence of positive or negative symptoms. In this report, we examine the evidence from brain pathology (enlargement of the cerebroventricular system, changes in gray and white matters, and abnormal laminar organization), genetics (changes in the normal expression of proteins that are involved in early migration of neurons and glia, cell proliferation, axonal outgrowth, synaptogenesis, and apoptosis), environmental factors (increased frequency of obstetric complications and increased rates of schizophrenic births due to prenatal viral or bacterial infections), and gene-environmental interactions (a disproportionate number of schizophrenia candidate genes are regulated by hypoxia, microdeletions and microduplications, the overrepresentation of pathogen-related genes among schizophrenia candidate genes) in support of the neurodevelopmental model. We relate the neurodevelopmental model to a number of findings about schizophrenia. Finally, we also examine alternate explanations of the origin of schizophrenia including the neurodegenerative model.

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“Thus, circuits tend to be malleable but vulnerable during postnatal development; notably, several neurodevelopmental disorders, such as ASD and SCZ, manifest during this plasticity period [49, 50].”
Background

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Authors: Fatemi, S. H., & Folsom, T. D.
Affiliations: University of Minnesota (US)
ORCID: Fatemi, S. H.
Venue: Schizophrenia Bulletin
Publisher: Oxford University Press (OUP)
Published: 2009-03-30
Volume: 35
Issue: 3
Pages: 528-548
ISSN: 0586-7614 (ISSN-L)
1745-1701
DOI: 10.1093/schbul/sbn187
PMC: PMC2669580
OpenAlex: W2132748057
Cited by: 860
References: 222
Citations by year: 2026: 23 · 2025: 46 · 2024: 47 · 2023: 42 · 2022: 39 · 2021: 48 · 2020: 45 · 2019: 40 · 2018: 43 · 2017: 48 · 2016: 61 · 2015: 53 · 2014: 55 · 2013: 76 · 2012: 66
FWCI: 8.07
Type: journal article
Language: en
Open access: bronze
doi.org
Locations: Schizophrenia Bulletin (publishedVersion)
Europe PMC (PubMed Central) (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Funders: National Institute of Child Health and Human Development
Eunice Kennedy Shriver National Institute of Child Health and Human Development (R01HD046589)
Topics: Health Sciences › Medicine › Psychiatry and Mental health › Schizophrenia research and treatment
Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
Social Sciences › Arts and Humanities › Philosophy › Mental Health and Psychiatry
Keywords: schizophrenia, neurodevelopmental hypothesis
MeSH terms: Adolescent, Adult, Animals, Brain, Disease Models, Animal, Female, Humans, Infant, Newborn, Mutation, Nerve Net, Pregnancy, Prenatal Exposure Delayed Effects, Risk Factors, Schizophrenia, Schizophrenic Psychology, Virus Diseases, Gene Expression, Neurodegenerative Diseases, Oligonucleotide Array Sequence Analysis, Young Adult

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The Neurodevelopmental Hypothesis of Schizophrenia, Revisited

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