Schizophrenia, "just the facts" what we know in 2008. 2. Epidemiology and etiology.

University of Florida, 3706 Glin Circle, Tallahassee, FL 32309, United States.
Schizophrenia Research (Impact Factor: 4.43). 08/2008; 102(1-3):1-18. DOI: 10.1016/j.schres.2008.04.011
Source: PubMed

ABSTRACT Although we have studied schizophrenia as a major disease entity over the past century, its causes and pathogenesis remain obscure. In this article, we critically review genetic and other epidemiological findings and discuss the insights they provide into the causes of schizophrenia. The annual incidence of schizophrenia averages 15 per 100,000, the point prevalence averages approximately 4.5 per population of 1000, and the risk of developing the illness over one's lifetime averages 0.7%. Schizophrenia runs in families and there are significant variations in the incidence of schizophrenia, with urbanicity, male gender, and a history of migration being associated with a higher risk for developing the illness. Genetic factors and gene-environment interactions together contribute over 80% of the liability for developing schizophrenia and a number of chromosomal regions and genes have been "linked" to the risk for developing the disease. Despite intensive research and spectacular advances in molecular biology, however, no single gene variation has been consistently associated with a greater likelihood of developing the illness and the precise nature of the genetic contribution remains obscure at this time. Environmental factors linked to a higher likelihood of developing schizophrenia include cannabis use, prenatal infection or malnutrition, perinatal complications, and a history of winter birth; the exact relevance or nature of these contributions is, however, unclear. How various genetic and environmental factors interact to cause schizophrenia and via which precise neurobiological mechanisms they mediate this effect is not understood. Etiological heterogeneity, complex patterns of gene-gene and gene-environment interaction, and inadequately elucidated schizophrenia pathophysiology are among the explanations invoked to explain our inadequate understanding of the etio-pathogenesis of schizophrenia. The ability to question some of our basic assumptions about the etiology and nature of schizophrenia and greater rigor in its study appear critical to improving our understanding about its causation.

1 Bookmark
  • Noropsikiyatri Arsivi 09/2011; 48(3):1-1. · 0.13 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Work and social functioning in schizophrenia are strongly influenced by cognitive impairment so improving cognition is a priority in the treatment of schizophrenia. Until recently the lack of a widely accepted index of cognitive change for use in schizophrenia was a major obstacle to the development of cognition enhancing treatments. The MATRICS (measurement and treatment research to improve cognition in schizophrenia) consensus cognitive battery (MCCB) was developed as a standard cognitive battery for use in clinical trials of cognition enhancing treatments for schizophrenia and has attracted worldwide interest. To analyze the reliability and validity of a translated and adapted Polish approved academic version of the MCCB. Sixty one patients were assessed at baseline and again after 30 days. The study protocol approximated the MATRICS psychometric and standardization study; the 10 tests that comprise the MCCB were administered to participants. Functioning and psychopathological symptoms were also assessed. Patients and test administrators also assessed the tolerability and practicality of all the cognitive tests. All tests in the battery were found to have high test-retest reliability. All the tests were rated as tolerable and practical by patients and administrators. However practice effects were generally higher in the Polish version of the MCCB than in the original version. Our analysis corroborates previous evidence that the MCCB represents a good tool for assessing cognitive deficits in research studies of schizophrenia also in non-English speaking countries.
    The Psychiatric quarterly. 01/2015;
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Throughout the scientific world the topic of cannabis usage and its link with psychosis seems to be discussed intensively. Considering the fact that the Czech Republic is a country with one of the highest prevalence of cannabis usage in the world it becomes a sensitive issue even in our circumstances. In the theoretical part of the work we attempted to review current knowledge of a link between cannabinoid system, canabis usage and psychosis and to point out possible future therapeutic potential of cannabinoids in the treatment of psychotic diseases. In the practical part of the work we focused on verification of propsychotic features of THC in animal model with particular attention to validation of acute subcutaneous admonistration of this drug as a novel cannabinoid model of psychosis. At the same time we tried to elucidate antipsychotic effect of CBD in this model. We tested these hypotheses in two behavioral tests (open field test, PPI ASR) and electrophysiologically (quantitative EEG). The whole analysis is enriched with pharmacokinetic data from subcutanneous and oral administration of cannabinoids.
    09/2014, Degree: Master's, Supervisor: Tomáš Páleníček

Full-text (2 Sources)

Available from
Aug 7, 2014