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Psychiatric Genetics (psychiatric + genetics)
Selected AbstractsAbstracts for the Xth World Congress of Psychiatric GeneticsAMERICAN JOURNAL OF MEDICAL GENETICS, Issue 7 2002Article first published online: 18 SEP 200 First page of article [source] Abstracts for the IXth World Congress of Psychiatric Genetics, Saint Louis, MissouriAMERICAN JOURNAL OF MEDICAL GENETICS, Issue 7 2001M.D., Richard Todd Ph.D. No abstract is available for this article. [source] From age correction to genome-wide associationACTA PSYCHIATRICA SCANDINAVICA, Issue 5 2009S. Cohen-Woods Objective:, Eric Strömgren was one of the pioneers of psychiatric genetics and family studies. There has now been an explosion of interest in this field and research progress, including linkage and association studies, whole genome genotyping, copy number variants and epigenetics is reviewed here. Method:, An overview of this area of psychiatric research is presented and discussed based on the relevant literature aiming at giving a recent status of the progress. Results:, Broadly speaking linkage and association are complementary approaches used to locate genes contributing to the genetic aetiology of psychopathology. Linkage can be detected over comparatively large distances, however power is problematic when searching for quantitative trait loci with small effect sizes. In contrast, association studies can detect small effects but only over very small distances. Therefore, while several genome-wide linkage studies in psychiatric disorders have been performed, the majority of association studies have investigated specific functional candidate genes. Conclusion:, Due to very recent technological advancements, genome-wide association studies have now become possible and have identified some completely novel susceptibility loci. Other recent advances include the discovery of epigenetic phenomena and copy number variants. [source] Schizophrenia: genetics, prevention and rehabilitationACTA NEUROPSYCHIATRICA, Issue 3 2009Paolo Olgiati Objective:, Genetic factors are largely implicated in predisposing to schizophrenia. Environmental factors contribute to the onset of the disorder in individuals at increased genetic risk. Cognitive deficits have emerged as endophenotypes and potential therapeutic targets for schizophrenia because of their association with functional outcome. The aims of this review were to analyse the joint effect of genetic and environmental (G×E) factors on liability to schizophrenia and to investigate relationships between genes and cognitive endophenotypes focusing on practical applications for prevention and rehabilitation. Methods:, Medline search of relevant studies published between 1990 and 2008. Results:, In schizophrenia, examples of G×E interaction include the catechol- O -methyl transferase (COMT) (Val158Met) polymorphism, which was found to moderate the onset of psychotic manifestations in response to stress and to increase the risk for psychosis related to cannabis use, and neurodevelopmental genes such as AKT1 (serine-threonine kinase), brain-derived neurotrophic factor (BDNF), DTNBP1 (dysbindin) and GRM3 (metabotropic glutamate receptor 3), which were associated with development of schizophrenia in adulthood after exposure to perinatal obstetric complications. Neurocognitive deficits are recognised as core features of schizophrenia that facilitate the onset of the disorder and have a great impact on functional outcome. Neurocognitive deficits are also endophenotypes that have been linked to a variety of genes [COMT, neuregulin (NRG1), BDNF, Disrupted-In-Schizophrenia 1 (DISC1) and dysbindin] conferring susceptibility to schizophrenia. Recently, it has emerged that cognitive improvement during rehabilitation therapy was under control of COMT (Val158Met) polymorphism. Conclusion:, This review could indicate a pivotal role of psychiatric genetics in prevention and rehabilitation of schizophrenic psychoses. [source] | ||||||||||