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.
| Original language | English |
|---|---|
| Pages (from-to) | 109-120 |
| Number of pages | 12 |
| Journal | Acta Neuropsychiatrica |
| Volume | 21 |
| Issue number | 3 |
| DOIs | |
| Publication status | Published - Jun 2009 |
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Keywords
- Endophenotypes
- Gene
- Prevention
- Rehabilitation
- Review
- Schizophrenia
ASJC Scopus subject areas
- Psychiatry and Mental health
- Biological Psychiatry
Cite this
Schizophrenia : Genetics, prevention and rehabilitation: Review article. / Olgiati, Paolo; Mandelli, Laura; Lorenzi, Cristina; Marino, Elena; Adele, Pirovano; Ferrari, Barbara; De Ronchi, Diana; Serretti, Alessandro.
In: Acta Neuropsychiatrica, Vol. 21, No. 3, 06.2009, p. 109-120.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Schizophrenia
T2 - Genetics, prevention and rehabilitation: Review article
AU - Olgiati, Paolo
AU - Mandelli, Laura
AU - Lorenzi, Cristina
AU - Marino, Elena
AU - Adele, Pirovano
AU - Ferrari, Barbara
AU - De Ronchi, Diana
AU - Serretti, Alessandro
PY - 2009/6
Y1 - 2009/6
N2 - 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.
AB - 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.
KW - Endophenotypes
KW - Gene
KW - Prevention
KW - Rehabilitation
KW - Review
KW - Schizophrenia
UR - http://www.scopus.com/inward/record.url?scp=68049131598&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=68049131598&partnerID=8YFLogxK
U2 - 10.1111/j.1601-5215.2009.00360.x
DO - 10.1111/j.1601-5215.2009.00360.x
M3 - Article
AN - SCOPUS:68049131598
VL - 21
SP - 109
EP - 120
JO - Acta Neuropsychiatrica
JF - Acta Neuropsychiatrica
SN - 0924-2708
IS - 3
ER -