@article{StoeberFranzekBeckmann1993,
  author    = {St{\"o}ber, Gerald and Franzek, E. and Beckmann, H.},
  title     = {Schwangerschafts- und Geburtskomplikationen - ihr Stellenwert in der Entstehung schizophrener Psychosen},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-63343},
  year      = {1993},
  abstract  = {In a retrospective study of 80 chronic DSM 111-R schizophrenics and 80 controls, the occurrence of obstetric complications (OCs) into the development of chronic schizophrenias was investigated using Leonhard s distinction in systematic schizophrenia (no obvious familial loading) and unsystematic schizophrenia (mainly genetically determined according to Leonhard). The Lewis \& Murray and Fuchs scales were used for evaluation. In both scales, unsystematic schizophrenias did not differ from controls, but those with OCs were significantly (p < 0.01) earlier hospitalized (20.5 years) than those without OCs (25.6 years). Systematic schizophrenics had an increased frequency, severity and total score of OCs compared to controls in the Fuchs scale (p < 0.0 I). Likewise, in the Lewis \& Murray scale systematic schizophrenia showed an increased presence ofOCs compared to controls (p < 0.05) and to unsystematic schizophrenia (p < 0.1 ). Systematic schizophrenias were significantly allocated to matemal infectious diseases during mid-gestation. Patients with matemal infections showed moreadditional OCs than those without (p < 0.05; Lewis \& Murray scale). In systematic schizophrenia, a history of OC was not associated with an early onset of the disease. In the genetic determined schizophrenias prenatal and perinatal disturbanccs Iead to an early onset of the disease, however, in systematic schizophrenias they seem to be of causal importance for the development of the disease.},
  subject      = {Schwangerschaft},
  language  = {en}
}
@article{StrikDierksFranzeketal.1994,
  author    = {Strik, Werner K. and Dierks, Thomas and Franzek, Ernst and St{\"o}ber, Gerald and Maurer, Konrad},
  title     = {P300 in Schizophrenia: Interactions between Amplitudes and Topography},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-63351},
  year      = {1994},
  abstract  = {Low P300 amplitudes and topographical asymmetries have been reponed in schizophrenic patients, but reference-independent amplitude assessment failed to replicate reduced amplitudes. P300 amplitude is conventially assessed at midline electrodes (PZ), anti asymmetric topography as reported in schizophrenics, may conj'ound this measurement. We lnvestigated the possible Interaction between P300 ropography and assessments of amplitudes. ln 41 clinically stable schizophrenics and 31 normal controls, the generalfinding ofreduced amplitudes at the P'l electrode and topographical asymmetrles in the patient group were replicated. ln both groups, a.symmetries of the P300 field (lateralized peaks) reduced the standard amplitude assessment at the midline parletal electrode, but did not Qjfoct the reference-independent, global amplitude assessment. This shows thal asymmetry per se does not imply reduced field strength. in addition, in schizophreraics. but not in controls, there was a significcmt effect oftlae direction of asymmetry on both amplltude measures, amplitudes belng lower with increasing shift ofthe P300 peak to the right side. Considering also the slightly left-lateralized peaks in the normal controls. this suggests rhat only right lateralized P300 peaks upressfunctional deficits in schizophrenics, whereas left lateralized pealcs fall wlthin the physiological variability of the P3OO field. Tht refonnce-independent amplitude assessment is proposed for unambiguous amplitude assessment in order to better define the clinical, psychological and physiopathological mtaning of the P3OO alterations in schizophrenics.},
  subject      = {Schizophrenie},
  language  = {en}
}
@article{LeschStoeberBallingetal.1994,
  author    = {Lesch, K. P. and St{\"o}ber, Gerald and Balling, U. and Franzek, Ernst and Li, S. H. and Ross, C. A. and Newman, M. and Beckmann, H. and Riederer, P.},
  title     = {Triplet repeats in clinical subtypes of schizophrenia: variation at the DRPLA (B37 CAG repeat) locus is not associated with periodic catatonia},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-63369},
  year      = {1994},
  abstract  = {Clinical evidence for a dominant mode of inheritance and anticipation in periodic catatonia, a distinct subtype of schizophrenia, indicates that genes with triplet repeat expansions or other unstable repetitive elements affecting gene expression may be involved in the etiology of this disorder. Because patients affected with dentatorubral-pallidoluysian atrophy (DRPLA) may present with "schizophrenic" symptoms, we have investigated the DRPLA (B 37 CAG repeat) locus on chromosome 12 in 41 patients with periodic catatonia. The B 37 CAG repeat locus was highly polymorphic but all alleles in both the patient and control group had repeat sizes within the normal range. We conclude that variation at the DRPLA locus is unlikely to be associated with periodic catatonia. The evidence for dominant inheritance and anticipation as well as the high prevalence of human brain genes containing trinucleotide repeats justifies further screening for triplet repeat expansions in periodic catatonia.},
  subject      = {Schizophrenie},
  language  = {en}
}
@article{StrikDierksFranzeketal.1994,
  author    = {Strik, Werner K. and Dierks, Thomas and Franzek, Ernst and St{\"o}ber, Gerald and Maurer, Konrad},
  title     = {P 300 asymmetries in schizophrenia revisited with reference-independent methods},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-63372},
  year      = {1994},
  abstract  = {Evidence of hemispheric asymmetries in schizophrenia has been reported from different research areas. Asymmetries in evoked potential P300 topography are still controversial because of inconsistent findings. In the present study. previous results of abnormal lateralization of P300 were replicated in stabilized residual Schizophrenie patients. Auditory P300 was recorded during an odd ball task in which subjeets detected rare target stimuli. Schizophrenie patients had the P300 peak shifted to the right hemisphere and differed signifieantly from age- and sex-matched normal control subjects who had left-lateralized P300 peaks. A comparison of different methods of assessment and analysis of the topographical features of the P300 electric fields showed that the extraction of reference-independent descriptors of P300 topography is a reliable and sensitive method for statistical handling of the maps. The results suggest left hemispheric dysfunction during cognitive tasks in a subgroup of Schizophrenie patients. Inconsistencies between previous sturlies are likely to be due to heterogeneous patient groups, which may have included patients in an acute Schizophrenie episode or patients in clinical remission. lnvestigation of the clinical meaning of P300 alterations requires careful psychopathological definition of the patient groups.},
  subject      = {Schizophrenie},
  language  = {en}
}
@article{RiveroReifSanjuanetal.2010,
  author    = {Rivero, Olga and Reif, Andreas and Sanjuan, Julio and Molto, Maria D. and Kittel-Schneider, Sarah and Najera, Carmen and Toepner, Theresia and Lesch, Klaus-Peter},
  title     = {Impact of the AHI1 Gene on the Vulnerability to Schizophrenia: A Case-Control Association Study},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-68501},
  year      = {2010},
  abstract  = {Background: The Abelson helper integration-1 (AHI1) gene is required for both cerebellar and cortical development in humans. While the accelerated evolution of AHI1 in the human lineage indicates a role in cognitive (dys)function, a linkage scan in large pedigrees identified AHI1 as a positional candidate for schizophrenia. To further investigate the contribution of AHI1 to the susceptibility of schizophrenia, we evaluated the effect of AHI1 variation on the vulnerability to psychosis in two samples from Spain and Germany. Methodology/Principal Findings: 29 single-nucleotide polymorphisms (SNPs) located in a genomic region including the AHI1 gene were genotyped in two samples from Spain (280 patients with psychotic disorders; 348 controls) and Germany (247 patients with schizophrenic disorders; 360 controls). Allelic, genotypic and haplotype frequencies were compared between cases and controls in both samples separately, as well as in the combined sample. The effect of genotype on several psychopathological measures (BPRS, KGV, PANSS) assessed in a Spanish subsample was also evaluated. We found several significant associations in the Spanish sample. Particularly, rs7750586 and rs911507, both located upstream of the AHI1 coding region, were found to be associated with schizophrenia in the analysis of genotypic (p = 0.0033, and 0.031,respectively) and allelic frequencies (p = 0.001 in both cases). Moreover, several other risk and protective haplotypes were detected (0.006,p,0.036). Joint analysis also supported the association of rs7750586 and rs911507 with the risk for schizophrenia. The analysis of clinical measures also revealed an effect on symptom severity (minimum P value = 0.0037). Conclusions/Significance: Our data support, in agreement with previous reports, an effect of AHI1 variation on the susceptibility to schizophrenia in central and southern European populations.},
  subject      = {Schizophrenie},
  language  = {en}
}
@article{GellaSeguraDuranyetal.2011,
  author    = {Gella, Alejandro and Segura, Monica and Durany, Nuria and Pfuhlmann, Bruno and Stoeber, Gerald and Gawlik, Micha},
  title     = {Is Ankyrin a specific genetic risk factor for psychiatric phenotypes?},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-68732},
  year      = {2011},
  abstract  = {Background: Genome wide association studies reported two single nucleotide polymorphisms in ANK3 (rs9804190 and rs10994336) as independent genetic risk factors for bipolar disorder. Another SNP in ANK3 (rs10761482) was associated with schizophrenia in a large European sample. Within the debate on common susceptibility genes for schizophrenia and bipolar disorder, we tried to investigate common findings by analyzing association of ANK3 with schizophrenia, bipolar disorder and unipolar depression. Methods: We genotyped three single nucleotide polymorphisms (SNPs) in ANK3 (rs9804190, rs10994336, and rs10761482) in a case-control sample of German descent including 920 patients with schizophrenia, 400 with bipolar affective disorder, 220 patients with unipolar depression according to ICD 10 and 480 healthy controls. Sample was further differentiated according to Leonhard's classification featuring disease entities with specific combination of bipolar and psychotic syndromes. Results: We found no association of rs9804190 and rs10994336 with bipolar disorder, unipolar depression or schizophrenia. In contrast to previous findings rs10761482 was associated with bipolar disorder (p = 0.015) but not with schizophrenia or unipolar depression. We observed no association with disease entities according to Leonhard's classification. Conclusion: Our results support a specific genetic contribution of ANK3 to bipolar disorder though we failed to replicate findings for schizophrenia. We cannot confirm ANK3 as a common risk factor for different diseases.},
  subject      = {Schizophrenie},
  language  = {en}
}