Aging and Error Processing: Age Related Increase in the Variability of the Error-Negativity Is Not Accompanied by Increase in Response Variability

Background: Several studies report an amplitude reduction of the error negativity (Ne or ERN), an event-related potential occurring after erroneous responses, in older participants. In earlier studies it was shown that the Ne can be explained by a single independent component. In the present study we aimed to investigate whether the Ne reduction usually found in older subjects is due to an altered component structure, i.e., a true alteration in response monitoring in older subjects. Methodology/Principal Findings: Two age groups conducted two tasks with different stimulus response mappings and task difficulty. Both groups received fully balanced speed or accuracy instructions and an individually adapted deadline in both tasks. Event-related potentials, Independent Component analysis of EEG-data and between trial variability of the Ne were combined with analysis of error rates, coefficients of variation of RT-data and ex-Gaussian fittings to reaction times. The Ne was examined by means of ICA and PCA, yielding a prominent independent component on error trials, the Ne-IC. The Ne-IC was smaller in the older than the younger subjects for both speed and accuracy instructions. Also, the Ne-IC contributed to a much lesser extent to the Ne in older than in younger subjects. RT distribution parameters were not related to Ne/ERP-variability. Conclusions/Significance: The results show a genuine reduction as well as a different component structure of the Ne in older compared to young subjects. This reduction is not reflected in behaviour, apart from a general slowing of olde

Phase-selective growth of κ\kappa- vs β\beta-Ga2_2O3_3 and (Inx_xGa1−x_{1-x})2_2O3_3 by In-mediated metal exchange catalysis in plasma-assisted molecular beam epitaxy

Its piezo- and potentially ferroelectric properties make the metastable kappa polymorph of Ga$_2$O$_3$ an interesting material for multiple applications, while In-incorporation into any polymorphs of Ga$_2$O$_3$ allows to lower their bandgap. In this work, we provide a guideline to achieve single phase $\kappa$-, $\beta$-Ga$_2$O$_3$ as well as their (In$_x$Ga$_{1-x}$)$_2$O$_3$ alloys up to x = 0.14 and x = 0.17 respectively, using In-mediated metal exchange catalysis in plasma assisted molecular beam epitaxy (MEXCAT-MBE). The polymorph transition from $\kappa$ to $\beta$ is also addressed, highlighting the fundamental role played by the thermal stability of the $\kappa$-Ga$_2$O$_3$. Additionally, we also demonstrate the possibility to grow ($\bar{2}$01) $\beta$-Ga$_2$O$_3$ on top of $\alpha$-Al$_2$O$_3$ (0001) at temperatures at least 100 {\deg}C above those achievable with conventional non-catalyzed MBE, opening the road for increased crystal quality in heteroepitaxy. The role of the substrate, as well as strain and structural defects in the growth of $\kappa$-Ga$_2$O$_3$ is also investigated by growing simultaneously on three different materials: (i) $\alpha$-Al$_2$O$_3$ (0001), (ii) 20 nm of ($\bar{2}$01) $\beta$-Ga$_2$O$_3$ on $\alpha$-Al$_2$O$_3$ (0001) and (iii) ($\bar{2}$01) $\beta$-Ga$_2$O$_3$ single crystal.Comment: Main text: 7 pages, 4 figures; Supplementary: 6 pages, 9 figure

Dopamine transporter (DAT1) and dopamine receptor D4 (DRD4) genotypes differentially impact on electrophysiological correlates of error processing

Peer reviewedPublisher PD

Response Monitoring in De Novo Patients with Parkinson's Disease

BACKGROUND: Parkinson's disease (PD) is accompanied by dysfunctions in a variety of cognitive processes. One of these is error processing, which depends upon phasic decreases of medial prefrontal dopaminergic activity. Until now, there is no study evaluating these processes in newly diagnosed, untreated patients with PD ("de novo PD"). METHODOLOGY/PRINCIPAL FINDINGS: Here we report large changes in performance monitoring processes using event-related potentials (ERPs) in de novo PD-patients. The results suggest that increases in medial frontal dopaminergic activity after an error (Ne) are decreased, relative to age-matched controls. In contrast, neurophysiological processes reflecting general motor response monitoring (Nc) are enhanced in de novo patients. CONCLUSIONS/SIGNIFICANCE: It may be hypothesized that the Nc-increase is at costs of dopaminergic activity after an error; on a functional level errors may not always be detected and correct responses sometimes be misinterpreted as errors. This pattern differs from studies examining patients with a longer history of PD and may reflect compensatory processes, frequently occurring in pre-manifest stages of PD. From a clinical point of view the clearly attenuated Ne in the de novo PD patients may prove a useful additional tool for the early diagnosis of basal ganglia dysfunction in PD