Enhancement of activity of the primary visual cortex during processing of emotional stimuli as measured with event-related functional near-infrared spectroscopy and event-related potentials

In this study we investigated whether event-related near-infrared spectroscopy (NIRS) is suitable to measure changes in brain activation of the occipital cortex modulated by the emotional content of the visual stimuli. As we found in a previous pilot study that only positive but not negative stimuli differ from neutral stimuli (with respect to oxygenated haemoglobin), we now measured the event-related EEG potentials and NIRS simultaneously during the same session. Thereby, we could evaluate whether the subjects (n = 16) processed the positive as well as the negative emotional stimuli in a similar way. During the task, the subjects passively viewed positive, negative, and neutral emotional pictures (40 presentations were shown in each category, and pictures were taken from the International Affective Picture System, IAPS). The stimuli were presented for 3 s in a randomized order (with a mean of 3 s interstimulus interval). During the task, we measured the event-related EEG potentials over the electrode positions O1, Oz, O2, and Pz and the changes of oxygenated and deoxygenated haemoglobin by multichannel NIRS over the occipital cortex. The EEG results clearly show an increased early posterior negativity over the occipital cortex for both positive as well as negative stimuli compared to neutral. The results for the NIRS measurement were less clear. Although positive as well as negative stimuli lead to significantly higher decrease in deoxygenated haemoglobin than neutral stimuli, this was not found for the oxygenated haemoglobin.     

Parkinson patient fibroblasts show increased alpha-synuclein expression

Parkinson's disease (PD) is a neurodegenerative movement disorder of advanced age with largely unknown etiology, but well documented tissue damage from oxidative stress. Increased α-synuclein (SNCA) expression is known to cause a rare form of PD, early-onset autosomal dominant PARK4. We have previously shown that loss-of-function mutations of the mitochondrial kinase PINK1 which cause the early-onset recessive PARK6 variant result in oxidative damage in patient fibroblasts. We now investigated the molecular chain of events from mitochondrial dysfunction to cell death which is largely unknown. Primary skin fibroblast cultures from patients were analysed for gene expression anomalies. In G309D-PINK1 patient fibroblasts, mainly genes regulated by oxidative stress, as well as genes encoding synaptic proteins such as SNCA showed altered expression. The induction of SNCA was also observed in control fibroblasts with knock-down of PINK1. The induction of SNCA expression was found to constitute a specific disease biomarker in sporadic PD patient fibroblasts. To understand the mechanism of this induction, we exposed control fibroblasts to oxidative, proteasomal and endoplasmic reticulum stress and were able to trigger the SNCA expression upregulation. Our data indicate that loss-of-function of PINK1 leads to enhanced alpha-synuclein expression and altered cell–cell contact. Alpha-synuclein induction might represent a common event for different variants of PD as well as a PD-specific trigger of neurodegeneration. We propose that the expression changes described might potentially serve as biomarkers that allow objective PD patient diagnosis in an accessible, peripheral tissue.     

Electrophysiological evidence for cortical abnormalities in obsessive-compulsive disorder - a replication study using auditory event-related P300 subcomponents

Neuroimaging studies in recent years suggest that cortical hyperactivity associated with more aroused cognitive processes and overfocussed attention is involved in the pathogenesis of obsessive-compulsive disorder (OCD), which was electrophysiologically supported by an own pilot-study in a small sample of stabilized OCD patients. To replicate this first finding, the hypothesis of cortical hyperactivity was studied by measuring auditory event-related P300 subcomponents, especially the amplitude of the P3a and P3b subcomponent, in a large sample of acutely ill and unmedicated patients with OCD. The P300 of 63 patients with OCD (30 males, 33 females, 33.7+/-10.2 years old; 25.4+/-5.4 points at Yale-Brown-Obsessive-Compulsive-Scale (Y-BOCS)) was separated with dipole source analysis (BESA) into their subcomponents P3a and P3b, and compared to the P300 subcomponents of 63 gender and age matched healthy controls. No difference in the amplitude of P3a was found, but OCD patients had significantly larger amplitudes of P3b than the healthy controls, which replicates the results of the pilot study. Once again, our findings point to a hyperactivated cortical state also of temporo-parietal and hippocampal regions in OCD.