The DOI matches its Crossref record; 222 of the 222 references it cites were found in a registry or an index.
The Neurodevelopmental Hypothesis of Schizophrenia, Revisited
Open accessAbstract
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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“symptoms do not manifest fully until late adolescence.1”
From Adolescent Onset of Cortical Disinhibition in Schizophrenia: Insights From Animal Models (2011) · cites this paper as [1]
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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
Metadata
- 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
- 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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