Project description:Major depressive disorders (MDD) exhibit cognitive dysfunction with respect to attention. The deficiencies in cognitive control of emotional information are associated with MDD as compared to healthy controls (HC). However, the brain mechanism underlying emotion that influences the attentional control in MDD necessitates further research. The present study explores the emotion-regulated cognitive competence in MDD at a dynamic attentional stage. Event-Related Potentials (ERPs) were recorded from 35 clinical MDD outpatients and matched HCs by applying a modified affective priming dot-probe paradigm, which consisted of various emotional facial expression pairs. From a dynamic perspective, ERPs combined with sLORETA results showed significant differences among the groups. In compared to HC, 100?ms MDD group exhibited a greater interior-prefrontal N100, sensitive to negative-neutral faces. 200?ms MDD showed an activated parietal-occipital P200 linked to sad face, suggesting that the attentional control ability concentrated on sad mood-congruent cognition. 300?ms, a distinct P300 was observed at dorsolateral parietal cortex, representing a sustained attentional control. Our findings suggested that a negatively sad emotion influenced cognitive attentional control in MDD in the early and late attentional stages of cognition. P200 and P300 might be predictors of potential neurocognitive mechanism underlying the dysregulated attentional control of MDD.
Project description:The capacity to suppress irrelevant incoming input, termed sensory gating, is one of the most investigated inhibitory processes associated with cognitive impairments due to aging. The aim of this study was to examine the influence of aging on sensory gating by using somatosensory event-related potentials (ERPs) elicited by repetitive non-painful tactile stimulation (paired-pulsed task). Somatosensory ERPs were recorded in 20 healthy young adults and 20 healthy older adults while they received two identical pneumatic stimuli (S1 and S2) of 100 ms duration with an inter-stimulus interval of 550 ± 50 ms on both forefingers. The difference between the somatosensory ERPs amplitude elicited by S1 and S2 was computed as a sensory gating measure. The amplitude and the latency of P50, N100 and late positive complex (LPC) were analyzed as well as the source generators of the gating effect. Reduced sensory gating was found in older individuals for N100 at frontal and centro-parietal electrodes and for LPC at fronto-central electrodes. Source localization analyses also revealed a reduced current density during gating effect in the older group in frontal areas in N100 and LPC. Moreover, older individuals showed delayed latencies in N100. No significant gating effect differences were found between groups in P50. These findings suggest an age-related slowing of processing speed and a reduced efficiency of inhibitory mechanisms in response to repetitive somatosensory information during stimulus evaluation, and a preservation of processing speed and inhibitory control during early stimulus coding in aging.
Project description:PurposeThe purpose of present study was to investigate the impact of sport experience on response inhibition and response re-engagement in expert badminton athletes during the stop-signal task and change-signal task.MethodsA total of 19 badminton athletes and 20 nonathletes performed both the stop-signal task and change-signal task. Reaction times (RTs) and event-related potentials were recorded and analyzed.ResultsBehavioral results indicated that badminton athletes responded faster than nonathletes to go stimuli and to change signals, with faster change RTs and change-signal RTs, which take into consideration the variable stimulus onset time mean. During successful change trials in the change-signal task, the amplitudes of the event-related potential components N2 and P3 were smaller for badminton athletes than for nonathletes. Moreover, change-signal RTs and N2 amplitudes as well as change RTs and P3 amplitudes were significantly correlated in badminton athletes. A significant correlation was also found between the amplitude of the event-related potential component N1 and response accuracy to change signals in badminton athletes.ConclusionModeration of brain cortical activity in badminton athletes was more associated with their ability to rapidly inhibit a planned movement and re-engage with a new movement compared with nonathletes. The superior inhibitory control and more efficient neural mechanisms in badminton athletes compared with nonathletes might be a result of badminton athletes' professional training experience.
Project description:Pervasive deficits of attention and set switching have been reported in schizophrenia, prompting efforts to identify the information processing mechanisms associated with these deficits. Recent evidence suggests that set switching may be intact in schizophrenia when the task switch requires only a change in the relevance of perceptual dimensions (e.g., attentional set switches) but decision-to-response mappings (intentional set) are maintained across trials in a cued task switching procedure. The goal of the present research was to replicate this finding and to test its direct corollary, which is the unconventional prediction that individuals with schizophrenia will evidence an intact, switch-sensitive P3(b) brain response to cued switches of attentional set. This prediction was tested in a group of 20 individuals with schizophrenia and 20 healthy comparison participants using event-related brain potential methodology and a cued task-switching task. Attentional set switching costs were equivalent between the two groups despite a set maintenance deficit in schizophrenia. Moreover, a posterior-parietal P3(b) component of the ERP was found to be equally sensitive to attentional set switching in schizophrenia and comparison groups, indicating a "healthy" brain response to switches of attentional set in schizophrenia. These results suggest that the dynamic control of attentional set may be preserved in schizophrenia and that previously reported executive deficits may be specific to the control of intentional task set and to deficits of task set maintenance.
Project description:BackgroundInhibition processing is sensitive to aging, and an age-related decline in inhibition processing has been associated with an accelerated rate of progression to Alzheimer disease. Elderly women are two to three times more likely than age-matched men to have Alzheimer disease. Therefore, this study examined whether long-term high physical activity affects inhibitory processing, specifically among postmenopausal women.MethodsIn total, 251 candidates were screened using the Montreal Cognitive Assessment and the Raven's Standard Progressive Matrices to assess their cognitive abilities and the International Physical Activity Questionnaire (Chinese version) to assess their physical activity levels. The participants were then grouped into either a long-term high physical activity group (defined as more than 3 days of high intensity activity per week and gross metabolic equivalent minutes (MET-minutes) higher than 1,500 MET-minutes/week or a gross MET higher than 3,000 MET-minutes/week obtained through walking or other moderate or high intensity activity) or a control group and matched for demographic and health characteristics as well as cognitive scores. Event-related potentials (ERPs) were recorded as participants performed a Go/No-go task to assess inhibition processing.ResultsThe long-term high physical activity group (n = 30) had faster Go reaction times than the control group (n = 30), whereas no significant difference between the two groups was found in their performance accuracy on the No-go task. For the ERP results, the latency of N2 component was significantly shorter in the long-term high physical activity group than that in the control group.DiscussionThe results of this study suggested that long-term high physical activity may increase the efficiency of the inhibitory control system by increasing the activity of response monitoring processes.
Project description:Contemporary models of substance use disorders emphasize the role of cognitive control, which has been linked to difficulties in resisting the use of substances. In the present study, we measured two aspects of cognitive control, response inhibition (operationalized by a Go/NoGo Task) and performance monitoring (operationalized by an Eriksen Flanker Task), in a group of young cannabis-use disorder (CUD) patients and compared these functions with two control groups (i.e. a group of cigarette smokers and a group of non-smokers). We employed both behavioural and electrophysiological measures. The results indicate that CUD patients displayed reduced NoGo-P3 event-related potentials compared with non-smoking controls, but not compared with smoking controls. In addition, CUD patients were slower on Go trials than both control groups. No other between-group electrophysiological or behavioural differences were observed. These results seem to suggest that CUD patients have problems related to response inhibition, but performance monitoring seems relatively unaffected.
Project description:Williams syndrome (WS) is a genetic disorder caused by a hemizygous microdeletion on chromosome 7q11.23. WS is associated with a compelling neurocognitive profile characterized by relative deficits in visuospatial function, relative strengths in face and language processing, and enhanced drive toward social engagement. We used a combined functional magnetic resonance imaging (fMRI) and event-related potential (ERP) approach to examine the neural basis of social responsiveness in WS participants to two types of social stimuli, negative (fearful) and positive (happy) emotional facial expressions. Here, we report a double dissociation consistent across both methods such that WS participants exhibited heightened amygdala reactivity to positive (happy) social stimuli and absent or attenuated amygdala reactivity to negative (fearful) social stimuli, compared with controls. The fMRI findings indicate that atypical social processing in WS may be rooted in altered development of disparate amygdalar nuclei that subserve different social functions. The ERP findings suggest that abnormal amygdala reactivity in WS may possibly function to increase attention to and encoding of happy expressions and to decrease arousal to fearful expressions. This study provides the first evidence that the genetic deletion associated with WS influences the function of the amygdala to be particularly responsive to socially appetitive stimuli.
Project description:The current body of evidence suggests that an aerobic exercise session has a beneficial effect on inhibitory control, whereas the impact of coordinative exercise on this executive function has not yet been examined in children with ADHD. Therefore, the present study aims to investigate the acute effects of aerobic and coordinative exercise on behavioral performance and the allocation of attentional resources in an inhibitory control task. Using a cross-over design, children with ADHD-combined type and healthy comparisons completed a Flanker task before and after 20min moderately-intense cycling exercise, coordinative exercise and an inactive control condition. During the task, stimulus-locked event-related potentials were recorded with electroencephalography. Both groups showed an increase of P300 amplitude and decrease of reaction time after exercise compared to the control condition. Investigating the effect of exercise modality, aerobic exercise led to greater increases of P300 amplitude and reductions in reaction time than coordinative exercise in children with ADHD. The findings suggest that a single exercise bout improves inhibitory control and the allocation of attentional resources. There were some indications that an aerobic exercise session seems to be more efficient than coordinative exercise in reducing the inhibitory control deficits that persist in children with ADHD.
Project description:ObjectivesMindfulness-based cognitive therapy (MBCT) can reduce anxiety and depression symptoms in adults with anxiety disorders, and changes in threat-related attentional bias may be a key mechanism driving the intervention's effects on anxiety symptoms. Event-related potentials (ERPs) can illuminate the physiological mechanism through which MBCT targets threat bias and reduces symptoms of anxiety. This preliminary study examined whether P1 ERP threat-related attentional bias markers in anxious adults change from pre- to post-MBCT delivered in-person or virtually (via Zoom) and investigated the relationship between P1 threat-related attentional bias markers and treatment response.MethodsPre- and post-MBCT, participants with moderate to high levels of anxiety (N = 50) completed a dot-probe task with simultaneous EEG recording. Analyses focused on pre- and post-MBCT P1 amplitudes elicited by angry-neutral and happy-neutral face pair cues, probes, and reaction times in the dot-probe task and anxiety and depression symptoms.ResultsPre- to post-MBCT, there was a significant reduction in P1-Probe amplitudes (d = .23), anxiety (d = .41) and depression (d = .80) symptoms, and reaction times (d = .10). Larger P1-Angry Cue amplitudes, indexing hypervigilance to angry faces, were associated with higher levels of anxiety both pre- and post-MBCT (d = .20). Post-MBCT, anxiety symptoms were lower in the in-person versus virtual group (d = .80).ConclusionsMBCT may increase processing efficiency and decreases anxiety and depression symptoms in anxious adults. However, changes in threat bias specifically were generally not supported. Replication with a comparison group is needed to clarify whether changes were MBCT-specific.Clinical trials registrationNCT03571386, June 18, 2018.Supplementary informationThe online version contains supplementary material available at 10.1007/s12671-022-01910-x.
Project description:Dysfunction in sensory information processing is a hallmark of many neurological disorders, including autism spectrum disorders, schizophrenia and Rett syndrome (RTT). Using mouse models of RTT, a monogenic disorder caused by mutations in MECP2, we found that the large-scale loss of MeCP2 from forebrain GABAergic interneurons led to deficits in auditory event-related potentials and seizure manifestation, whereas the restoration of MeCP2 in specific classes of interneurons ameliorated these deficits.