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BackgroundIntellectual deficits are commonly found in schizophrenia patients. These intellectual deficits have been found to be heritable. However, whether the intellectual deficits change over time and, if so, whether the change is related with an increased genetic risk for the disease are not known.MethodWe investigated change of intelligence quotient (IQ) in a twin sample of chronically ill schizophrenia patients, the discordant co-twins and healthy controls during a follow-up period of 5 years. A total of 52 twins completed two IQ assessments: nine patients [three monozygotic (MZ) and six dizygotic (DZ)], 10 unaffected co-twins (three MZ and seven DZ) and 33 healthy control twins (21 MZ and 12 DZ).ResultsA significant interaction effect over time was found between IQ measurement and illness (F=4.22, df=1, pt=2.06, pt=−2.32, pt=−0.49, p=0.63).ConclusionsPatients with schizophrenia in the chronic phase of the disease, but not the discordant co-twins, show a lack of increase in IQ, which is probably due to environmental (non-genetic) factors related to the disease.

Background. Autism is a neurodevelopmental disorder with an estimated genetic origin of 90%. Previous studies have reported an increase in brain volume of approximately 5% in autistic subjects, especially in children. If this increase in brain volume is genetically determined, biological parents of autistic probands might be expected to show brain enlargement, or at least intracranial enlargement, as well. Identifying structural brain abnormalities under genetic control is of particular importance as these could represent endophenotypes of autism.Method. Using quantitative anatomic brain magnetic resonance imaging, volumes of intracranial, total brain, frontal, parietal, temporal and occipital lobe, cerebral and cortical gray and white matter, cerebellum, lateral ventricle, and third ventricle were measured in biological, non-affected parents of autistic probands (19 couples) and in healthy, closely matched control subjects (20 couples).Results. No significant differences were found between the parents of the autistic probands and healthy control couples in any of the brain volumes. Adding gender as a factor in a second analysis did not reveal a significant interaction effect of gender by group.Conclusions. The present sample of biological, non-affected parents of autistic probands did not show brain enlargements. As the intracranium is not enlarged, it is unlikely that the brain volumes of the parents of autistic probands have originally been enlarged and have been normalized. Thus, increased brain volume in autism might be caused by the interaction of paternal and maternal genes, possibly with an additional effect of environmental factors, or increased brain volumes might reflect phenotypes of autism.

Introduction In the recent years, interest of researchers has been focused on exercise as a possible way to efficiently influence brain functions and plasticity. Several studies concluded that exercise can change brain morphology by affecting synapses, neurogenesis and angiogenesis and improve efficiency in working memory and executive performance. In schizophrenia, white matter integrity is compromised and to what extent exercise affects white matter integrity is unclear. Aims To investigate the effect of 6 months exercise therapy on white matter integrity in healthy controls and patients with schizophrenia. Methods A total of 33 patients with schizophrenia and 48 healthy controls, matched for demographic characteristics, were randomized into exercise or occupational therapy/life-as-usual. 3T-DTI data were acquired twice. After susceptibility-artifacts and ECC correction, TBSS was used for registration to standard space and computation of the FA-skeleton. The JHU-ICBM-tract atlas was used to define regions of interest (ROI) for the various fiber tracts. Mean FA values for the FA-skeleton within the separate tract ROIs were calculated. GLM-repeated measures design was done with time as within-subject factor, group and therapy as between-factors, and compliance as covariate. Results Significant increases in FA were found for time by randomization in the left corticospinal tract (LCST) (F=4,15, p=0,045), left superior longitudinal fascicle (LSLF)(F=5,092, p=0,027) and forceps major (F=5,687, p=0,02). Conclusions Exercise positively affects FA of tracts involved in primary motor functions (LCST), regulation of motor behavior, spatial attention, oculomotor functions and transfer of somatosensory information (LSLF) as well as interhemispheric connections (Forceps major) in both groups.

The genetic risk for schizophrenia is estimated to range between 60% and 80%. These estimates are based on family-studies. Patients with schizophrenia have changes in brain structure and function, Since brain structure and function are considerably heritable and include genes implicated in schizophrenia, these measures are interesting to provide phenotypic characterization of risk variant carriers. Indeed, it was found that first-degree family members of patients share some of the gray matter changes with the probands, and in particular those with increased genetic burdening such as in discordant twins of patients (Moran et al, 2013). A study in monozygotic and dizygotic twins discordant for schizophrenia revealed that local cortical thickness changes as well as smaller white matter volume in schizophrenia are for a considerable part heritable, including genes overlapping with the genetic risk for the disease (Hulshoff Pol et al, 2012). To determine whether the smaller white matter volume as a candidate endophenotype for schizophrenia reflects changes in white matter microstructure and network properties is an important next step. Brain measures may provide clinically relevant risk scores in the future. The feasibility to use a classification model based on magnetic resonance brain images (Schnack et al, in preparation), and to include family related contextual information (Mandl et al, 2013) to measure risk for schizophrenia will be discussed.

IntroductionStructural brain abnormalities have consistently been found in schizophrenia, with increased familial risk for the disease associated with these abnormalities. Some brain volume changes are progressive over the course of the illness.ObjectiveTo investigate whether these progressive brain volume changes are mediated by genetic or disease-related factors.MethodsWe carried out a 5-year follow-up study in monozygotic (MZ) and dizygotic (DZ) twin pairs discordant for schizophrenia (DISC) and healthy comparison (HC) twin pairs using brain magnetic resonance imaging. A total of 92 participants completed the study (DISC: 9 MZ and 10 DZ; HC: 14 MZ and 13 DZ). Percentage volume changes of the whole brain and cerebral gray and white matter were estimated. Structural equation modeling was applied to estimate contributions of additive genetic and common and unique environmental factors.ResultsSignificant decreases over time in whole brain volume was found in patients with schizophrenia and their unaffected co-twins compared with control twins. Bivariate structural equation modeling using cross-trait/cross-twin correlations revealed significant additive genetic influences on the correlations between schizophrenia liability and progressive whole brain (66%; 95% confidence interval [CI], 51%-100%), frontal lobe (76%; 95% CI, 54%-100%), and temporal lobe (79%; CI, 56%-100%) volume change.ConclusionsThe progressive brain volume loss found in patients with schizophrenia and their unaffected co-twins is at least partly attributable to genetic factors related to the illness.