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People suffering from depression perceive themselves and their surroundings as more negative than healthy ones. An explanation might be that depressed individuals experience negative information as more stressful than non-depressed subjects and, consequently, respond in an amplified manner on a subjective and physiological level. To test this proposition, we presented 41 patients with recurrent depressive episodes and 42 controls with stimuli from the International Affective Picture System split into three valence categories while different parameters of physiological arousal (e.g., heart rate variability) and subjective perceptions of valence and arousal were assessed. Furthermore, we examined social skills and emotional competence. Results regarding physiological arousal revealed an elevated skin temperature and a more accentuated respiratory frequency in depressed subjects. Furthermore, depressed subjects rated the stimuli as more negative and arousing, which was associated with reduced social and emotional competence. Variation in antidepressant medication, menstrual cycle and other factors that have an impact on HRV are a potential bias. Our findings suggest an intensified perception of negative emotion in depressed individuals as compared to controls that manifests itself in an increased physiological arousal as well as on a subjective level. This intensified emotion perception is further associated with deficits in social and emotional competence., final draft, peerReviewed

Cognitive impairments have been linked to structural and functional alterations in frontal and subcortical brain regions, ultimately leading to fronto-thalamic connectivity disturbances. We hypothesized that such neuronal disruptions in frontal and subcortical structures may account for neuropsychological deficits in schizophrenia (SZ), schizophrenia relatives and bipolar disorder (BD). We acquired T1-weighted anatomical MRI sequences in 209 participants: 57 SZ patients, 47 first-degree relatives of SZ patients, 48 BD I patients and 57 healthy controls. We computed group comparisons of gray matter (GM) volume in frontal and basal ganglia regions-of-interest, followed by correlation analysis between psychomotor speed, executive functioning and learning and GM volumes in candidate regions. Several frontal GM volume reductions as well as GM increases in the thalamus and the putamen were exhibited in SZ patients as compared to controls. The same finding was observed - less pronounced - when comparing SZ relatives and controls. BD patients presented GM volume increases in the basal ganglia in comparison to controls. In SZ patients, increases in bilateral thalamus GM volume and decreases in left middle and superior frontal gyrus volume were significantly associated with worse cognitive performance. In summary, our results indicate distinct imbalances across frontal-subcortical circuits in BD, SZ relatives and SZ. The functional relevance of the findings were mainly limited to the SZ patients group: in this group, abnormalities were directly associated with cognitive performance. This result is in line with the finding that the volume alterations were strongest in SZ patients and followed by BD patients and SZ relatives.

Proteomic analyses facilitate the interpretation of molecular biomarker probes which are very\ud helpful in diagnosing schizophrenia. In the current study, we attempt to test whether potential\ud differences in plasma protein expressions in schizophrenia (SZ) and bipolar disorder (BD) are\ud associated with cognitive deficits and their underlying brain structures.\ud 42 plasma proteins of 29 SZ patients, 25 BD patients and 93 non-clinical controls were\ud quantified and analysed using multiple reaction monitoring (MRM) based triple quadrupole\ud mass spectrometry approach. We also computed group comparisons of protein expressions\ud between patients and controls, and between SZ and BD patients, as well. Potential associations\ud of protein levels with cognitive functioning (psychomotor speed, executive functioning,\ud crystallized intelligence) as well as underlying brain volume in the hippocampus were explored,\ud using bivariate correlation analyses.\ud The main finding of this study was that apolipoprotein (ApoC) expression differed\ud between patients and controls; and that these alterations in both disease groups were putatively\ud related to cognitive impairments as well as to hippocampus volumes. However, none of the\ud protein level differences were related to clinical symptom severity.\ud In summary, altered apolipoprotein expression in BD and SZ was linked to cognitive\ud decline and underlying morphological changes in both disorders. Our results suggest that the\ud detection of molecular patterns in association with cognitive performance and its underlying\ud brain morphology is of great importance for understanding of the pathological mechanisms of\ud SZ and BD, as well as for supporting the diagnosis and treatment of both disorders.

BACKGROUND: Bipolar affective disorder (BD) is often associated with cognitive dysfunction in executive domains. However the biological underpinnings of cognitive deficits in BD are not sufficiently understood. A growing body of evidence indicates a loss of microstructural integrity in various white matter (WM) fiber tracts in BD. The aim of the current study was to assess potential links between WM structural abnormalities and cognitive performance in euthymic middle-aged BD patients (n=30) and matched healthy controls (n=32). METHODS: Diffusion tensor imaging (DTI) data was carried out with both voxelwise (tract based spatial statistics, TBSS) and region-of-interest (ROI) based analysis. We compared multiple indices of diffusion including fractional anisotropy (FA), radial (DR), axial (DA) and mean diffusivities (MD). RESULTS: Increased mean diffusivity was found in the fornix, anterior thalamic radiation, splenium and the truncus of the corpus callosum in BD patients compared with controls. These diffusion changes were significantly associated with poorer performance in executive tasks in BD patients. CONCLUSIONS: Our results indicate a direct link between executive cognitive functioning and abnormal WM microstructural integrity of fronto-limbic tracts in remitted BD patients, and add evidence to the neuronal disruption that underlies the residual symptomatology of BD.

A potential clinical and etiological overlap between schizophrenia (SZ) and bipolar disorder (BD) has long been a subject of discussion. Imaging studies imply functional and structural alterations of the hippocampus in both diseases. Thus, imaging this core memory region could provide insight into the pathophysiology of these disorders and the associated cognitive deficits. To examine possible shared alterations in the hippocampus, we conducted a multi-modal assessment, including functional and structural imaging as well as neurobehavioral measures of memory performance in BD and SZ patients compared with healthy controls. We assessed episodic memory performance, using tests of verbal and visual learning (HVLT, BVMT) in three groups of participants: BD patients (n = 21), SZ patients (n = 21) and matched (age, gender, education) healthy control subjects (n = 21). In addition, we examined hippocampal resting state functional connectivity, hippocampal volume using voxel-based morphometry (VBM) and fibre integrity of hippocampal connections using diffusion tensor imaging (DTI). We found memory deficits, changes in functional connectivity within the hippocampal network as well as volumetric reductions and altered white matter fibre integrity across patient groups in comparison with controls. However, SZ patients when directly compared with BD patients were more severely affected in several of the assessed parameters (verbal learning, left hippocampal volumes, mean diffusivity of bilateral cingulum and right uncinated fasciculus). The results of our study suggest a graded expression of verbal learning deficits accompanied by structural alterations within the hippocampus in BD patients and SZ patients, with SZ patients being more strongly affected. Our findings imply that these two disorders may share some common pathophysiological mechanisms. The results could thus help to further advance and integrate current pathophysiological models of SZ and BD., Highlights • multimodal assessment of the hippocampus formation. • comparison of bipolar patients, schizophrenia patients and controls. • assessment of associations beetween hippocampus alterations and cognitive functioning.