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Schizophrenia: genetics, prevention and rehabilitation

Published online by Cambridge University Press:  24 June 2014

Paolo Olgiati
Affiliation:
Department of Psychiatry, Institute of Psychiatry, Bologna University, Italy
Laura Mandelli
Affiliation:
Department of Psychiatry, Institute of Psychiatry, Bologna University, Italy
Cristina Lorenzi
Affiliation:
Department of Psychiatry, Istituto Scientifico San Raffaele, Vita-Salute University, Milan, Italy
Elena Marino
Affiliation:
Department of Psychiatry, Istituto Scientifico San Raffaele, Vita-Salute University, Milan, Italy
Pirovano Adele
Affiliation:
Department of Psychiatry, Istituto Scientifico San Raffaele, Vita-Salute University, Milan, Italy
Barbara Ferrari
Affiliation:
Department of Psychiatry, Institute of Psychiatry, Bologna University, Italy
Diana De Ronchi
Affiliation:
Department of Psychiatry, Institute of Psychiatry, Bologna University, Italy
Alessandro Serretti*
Affiliation:
Department of Psychiatry, Institute of Psychiatry, Bologna University, Italy
*
Alessandro Serretti, Institute of Psychiatry, University of Bologna, Viale Carlo Pepoli 5, 40123 Bologna, Italy. Tel: +39 051 6584233; Fax: +39 051 521030; E-mail: [email protected]

Abstract

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.

Type
Review article
Copyright
Copyright © 2009 John Wiley & Sons A/S

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