I Epidemiology of Schizophrenia- Deviant Birth Season Distribution: Does It Offer a Clue to the Aetiology of Schizophrenia?- Gender Differences in Age at Onset and Course of Schizophrenic Disorders A Contribution to the Understanding of the Disease?- Early Predictors of Onset and Course of Schizophrenia and Schizophrenia Spectrum- Epidemiology of Schizophrenia: Discussion- II Determinants of Course and Outcome of Schizophrenia- The International Pilot Study of Schizophrenia: Five-Year Follow-Up Findings- What Is Crucial for the Long-Term Outcome of Schizophrenia?- Models for the Development of Symptomatology and Course of Schizophrenia- Interaction of Environment and Personality in the Course of Schizophrenia- III Genetics of Schizophrenia- Models of Heritability and Genetic Transmission- Gene-Environment Interaction in Adoptive Families- The Reverse Genetic Approach to the Etiology of Schizophrenia- Genetics of Schizophrenia: Discussion- IV Vulnerability Models for Schizophrenia- Testing Vulnerability Models: Stability of Potential Vulnerability Indicators Across Clinical State- The Contributions of Psychophysiology to Vulnerability Models- The Contributions of Cognitive Psychology to Vulnerability Models- Vulnerability Models for Schizophrenia: Discussion- V Brain Anatomy in Schizophrenia- The Neuropathology of Schizophrenia- Computer Tomographic Studies in Schizophrenia- Magnetic Resonance Imaging of the Brain: Clinical and Research Applications in Schizophrenia- Brain Anatomy in Schizophrenia: Discussion- VI Brain Function in Schizophrenia- Positron Emission Tomography in Schizophrenia- Brain Localisation and Neuropsychology in Schizophrenia: Syndrome and Neurodevelopmental Implications- The Autonomic Orienting Response as a Possible Vulnerability Marker in Schizophrenia- Event-Related Potentials and Cognitive Dysfunction in Schizophrenia- Brain Function in Schizophrenia: Discussion- VII Future Strategies and Perspectives in Schizophrenia Research- Antipsychotic Drugs as Tools for Etiological Research- Strategies for Biological Research: Psychosis as an Anomaly of the Cerebral Dominance Gene- Strategies for Psychosocial Research into the Causes of Schizophrenia- New Perspectives in the Epidemiology of Schizophrenia- Future Strategies and Perspectives in Schizophrenia Research: Discussion- Closing Remarks- Author Index

Search for the Causes of Schizophrenia

OBJECTIVE: The authors assess implications of DSM criteria for schizophrenia by reviewing the criteria’s 1) emphasis on psychotic features, 2) dissociation of symptoms from their etiology, 3) exclusive reliance on clinical features but exclusion of biological indicators, and 4) classification of schizophrenia as a discrete category. The authors then discuss alternative conceptions of schizophrenia that take into account recent data concerning its genetic and neurodevelopmental origins and its pathophysiological substrates.METHOD: The historical development of diagnostic criteria for schizophrenia is reviewed in the context of recent published data on the biology and development of schizophrenia.RESULTS: Growing evidence suggests that symptoms of psychosis may be a common end-state in a variety of disorders, including schizophrenia, rather than a reflection of the specific etiology of schizophrenia. Features occurring before the advent of psychosis that are clinical, biological, and/or neuropsychological i...

Toward reformulating the diagnosis of schizophrenia.

Genetic epidemiology has provided consistent evidence over many years that schizophrenia has a genetic component, and that this genetic component is complex, polygenic, and involves epistatic interaction between loci. Molecular genetics studies have, however, so far failed to identify any DNA variant that can be demonstrated to contribute to either liability to schizophrenia or to any identifiable part of the underlying pathology. Replication studies of positive findings have been difficult to interpret for a variety of reasons. First, few have reproduced the initial findings, which may be due either to random variation between two samples in the genetic inputs involved, or to a lack of power to replicate an effect at a given alpha level. Where positive data have been found in replication studies, the positioning of the locus has been unreliable, leading no closer to positional cloning of genes involved. However, an assessment of all the linkage studies performed over the past ten years does suggest a number of regions where positive results are found numerous times. These include regions on chromosomes 1, 2, 4, 5, 6, 7, 8, 9, 10, 13, 15, 18, 22 and the X. All of these data are critically reviewed and their locations compared. Reasons for the difficulty in obtaining consistent results and possible strategies for overcoming them are discussed. Am. J. Med. Genet. (Semin. Med. Genet.) 97:23–44, 2000. © 2000 Wiley-Liss, Inc.

Linkage and associated studies of schizophrenia.

The case for heterogeneity in the etiology of schizophrenia

A systems approach to understanding the etiology of schizophrenia requires a theory which is able to integrate genetic as well as neurodevelopmental factors. 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. Supported by informed conjectures and empirical facts, the hypothesis makes an attractive case for a large number of further investigations. 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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The glial growth factors deficiency and synaptic destabilization hypothesis of schizophrenia

A susceptibility locus for schizophrenia in the 'pseudo-autosomal' region has been proposed on the basis of the reported excess of sex-chromosome aneuploidies (e.g. XXY and XXX) among patients with schizophrenia and the finding that schizophrenic sib-pairs are more often of the same than of the opposite sex. This hypothesis has been tested in 83 sibships with two or more siblings fulfilling Research Diagnostic Criteria for schizophrenia or schizoaffective disorder. Alleles at the pseudo-autosomal telomeric locus DXYS14, which is unlinked with sex, were analysed using the method of affected sib-pairs. Affected sibs shared alleles at DXYS14 more frequently than expected by random Mendelian assortment, supporting genetic linkage between DXYS14 and schizophrenia.

Evidence for a pseudo-autosomal locus for schizophrenia using the method of affected sibling pairs.

method of affected sibling pairs. Evidence for a pseudo-autosomal locus for schizophrenia using the

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Evidence for a pseudo-autosomal locus for schizophrenia using the method of affected sibling pairs.

method of affected sibling pairs. Evidence for a pseudo-autosomal locus for schizophrenia using the