| Hauptseite > Publikationsdatenbank > Identification of increased genetic risk scores for schizophrenia in treatment-resistant patients > print |
| 001 | 154144 | ||
| 005 | 20210129213837.0 | ||
| 024 | 7 | _ | |a 10.1038/mp.2014.56 |2 doi |
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| 037 | _ | _ | |a FZJ-2014-03537 |
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| 100 | 1 | _ | |0 P:(DE-HGF)0 |a Frank, J. |b 0 |e Corresponding Author |
| 245 | _ | _ | |a Identification of increased genetic risk scores for schizophrenia in treatment-resistant patients |
| 260 | _ | _ | |a London |b Macmillan |c 2015 |
| 336 | 7 | _ | |0 PUB:(DE-HGF)16 |2 PUB:(DE-HGF) |a Journal Article |b journal |m journal |s 1427449481_8870 |
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| 520 | _ | _ | |a Schizophrenia is a severe neuropsychiatric disorder that affects around 0.5–1% of the population. Research has shown that early intervention increases the likelihood of remission and reduces the severity of symptoms, as well as attenuates the decline in social and overall functioning.1Around 30% of patients fail to respond adequately to the usual antipsychotic medications, and are classified as being treatment resistant. These patients can be treated with the atypical antipsychotic clozapine, the only evidence-based pharmacotherapy for treatment-resistant schizophrenia. However, clozapine is associated with severe adverse events and is thus only prescribed in patients who have failed to respond to trials of two other antipsychotics. This process may take many years. Since an extended duration of untreated psychosis and lack of efficacy for the initial treatment are however associated with a poorer prognosis,6 identification of patients who will eventually require clozapine is an important goal for improving clinical outcome. Research to identify clinical predictors of response prior to treatment initiation has shown that premorbid social functioning (PSF) is among the most reliable measures (for a review see Schennach et al.6). Furthermore, reports of an association between a family history of psychosis and an unfavourable treatment response7 suggest the influence of genetic factors. However, few candidate gene studies have been conducted and their results are inconsistent. |
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| 700 | 1 | _ | |0 P:(DE-HGF)0 |a Lang, M. |b 1 |
| 700 | 1 | _ | |0 P:(DE-HGF)0 |a Witt, S. H. |b 2 |
| 700 | 1 | _ | |0 P:(DE-HGF)0 |a Strohmaier, J. |b 3 |
| 700 | 1 | _ | |0 P:(DE-HGF)0 |a Rujescu, D. |b 4 |
| 700 | 1 | _ | |0 P:(DE-Juel1)140234 |a Cichon, S. |b 5 |
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| 700 | 1 | _ | |0 P:(DE-HGF)0 |a Naber, D. |b 10 |
| 700 | 1 | _ | |0 P:(DE-HGF)0 |a Rietschel, M. |b 11 |e Corresponding Author |
| 773 | _ | _ | |0 PERI:(DE-600)1502531-7 |a 10.1038/mp.2014.56 |p 150-151 |t Molecular psychiatry |v 20 |x 1476-5578 |y 2015 |
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