ArticleBMC psychiatry2002
The glial growth factors deficiency and synaptic destabilization hypothesis of schizophrenia.
Article in BMC psychiatry, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 2 of them syntheses that pooled it.
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Who cites it
44 citing papers in PubMed, 2 syntheses or guidelines pooled it, 127 citations in OpenAlex.
- Postmortem evidence of brain inflammatory markers in bipolar disorder: a systematic review.Molecular psychiatry · 2020Pooled it
- Effect of Rhesus D incompatibility on schizophrenia depends on offspring sex.Schizophrenia research · 2008Pooled it
- Morphogenetic theory of mental and cognitive disorders: the role of neurotrophic and guidance molecules.Frontiers in molecular neuroscience · 2024Review
- Rats, Neuregulins and Radical Prostatectomy: A Conceptual Overview.Journal of clinical medicine · 2023Review
- Acetylcholine receptor subunit expression in Huntington's disease mouse muscle.Biochemistry and biophysics reports · 2021Article
- Association of Glial Cell-Line Derived Neurotrophic Factor and Nerve Growth Factor with Duration of Untreated Psychosis and Clinical Symptoms in Drug-Naive Schizophrenia.Psychiatry and clinical psychopharmacology · 2021Article
- Dysregulation of Fibroblast Growth Factor 10 in the Peripheral Blood of Patients with Schizophrenia.Journal of molecular neuroscience : MN · 2019Article
- GFRA1: A Novel Molecular Target for the Prevention of Osteosarcoma Chemoresistance.International journal of molecular sciences · 2018Review
- Immediate Early Genes Anchor a Biological Pathway of Proteins Required for Memory Formation, Long-Term Depression and Risk for Schizophrenia.Frontiers in behavioral neuroscience · 2018Article
- The Immediate Early GeneFrontiers in behavioral neuroscience · 2018Article
- Article
- Genetic evidence for role of integration of fast and slow neurotransmission in schizophrenia.Molecular psychiatry · 2017Review
- A novel relationship for schizophrenia, bipolar and major depressive disorder Part 5: a hint from chromosome 5 high density association screen.American journal of translational research · 2017Article
- Frontotemporal White Matter in Adolescents with, and at-Risk for, Bipolar Disorder.Journal of clinical medicine · 2014Review
- Neuropathological changes in the nucleus basalis in schizophrenia.European archives of psychiatry and clinical neuroscience · 2013Article
- Family-based association study of early growth response gene 3 with child bipolar I disorder.Journal of affective disorders · 2012Article
- The Role of Astrocytes in Metabolism and Neurotoxicity of the Pyrrolizidine Alkaloid Monocrotaline, the Main Toxin of Crotalaria retusa.Frontiers in pharmacology · 2012Article
- Neuregulin-1β for the treatment of systolic heart failure.Journal of molecular and cellular cardiology · 2011Review
- Diffusion tensor imaging, structural connectivity, and schizophrenia.Schizophrenia research and treatment · 2011Article
- Prolactin-a biomarker for antipsychotic treatment response?The primary care companion for CNS disorders · 2011Article
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundA systems approach to understanding the etiology of schizophrenia requires a theory which is able to integrate genetic as well as neurodevelopmental factors. PRESENTATION OF THE HYPOTHESIS: Based on a co-localization of loci approach and a large amount of circumstantial evidence, we here propose that a functional deficiency of glial growth factors and of growth factors produced by glial cells are among the distal causes in the genotype-to-phenotype chain leading to the development of schizophrenia. These factors include neuregulin, insulin-like growth factor I, insulin, epidermal growth factor, neurotrophic growth factors, erbB receptors, phosphatidylinositol-3 kinase, growth arrest specific genes, neuritin, tumor necrosis factor alpha, glutamate, NMDA and cholinergic receptors. A genetically and epigenetically determined low baseline of glial growth factor signaling and synaptic strength is expected to increase the vulnerability for additional reductions (e.g., by viruses such as HHV-6 and JC virus infecting glial cells). This should lead to a weakening of the positive feedback loop between the presynaptic neuron and its targets, and below a certain threshold to synaptic destabilization and schizophrenia. TESTING THE HYPOTHESIS: Supported by informed conjectures and empirical facts, the hypothesis makes an attractive case for a large number of further investigations. IMPLICATIONS OF THE HYPOTHESIS: The hypothesis suggests glial cells as the locus of the genes-environment interactions in schizophrenia, with glial asthenia as an important factor for the genetic liability to the disorder, and an increase of prolactin and/or insulin as possible working mechanisms of traditional and atypical neuroleptic treatments.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.