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• LPA promotes the migration of skeletal muscle-isolated FAPs through LPA 1 signaling. • YAP activity is required for LPA-induced migration of FAPs. • FAPs isolated from dystrophic muscle possess an enhanced migration response to LPA, behavior which can be blocked by inhibiting LPA 1/3 or YAP activity. Skeletal muscle fibrosis is defined as the excessive accumulation of extracellular matrix (ECM) components and is a hallmark of muscular dystrophies. Fibro-adipogenic progenitors (FAPs) are the main source of ECM, and thus have been strongly implicated in fibrogenesis. In skeletal muscle fibrotic models, including muscular dystrophies, FAPs undergo dysregulations in terms of proliferation, differentiation, and apoptosis, however few studies have explored the impact of FAPs migration. Here, we studied fibroblast and FAPs migration and identified lysophosphatidic acid (LPA), a signaling lipid central to skeletal muscle fibrogenesis, as a significant migration inductor. We identified LPA receptor 1 (LPA 1) mediated signaling as crucial for this effect through a mechanism dependent on the Hippo pathway, another pathway implicated in fibrosis across diverse tissues. This cross-talk favors the activation of the Yes-associated protein 1 (YAP) and Transcriptional coactivator with PDZ-binding motif (TAZ), leading to increased expression of fibrosis-associated genes. This study reveals the role of YAP in LPA-mediated fibrotic responses as inhibition of YAP transcriptional coactivator activity hinders LPA-induced migration in fibroblasts and FAPs. Moreover, we found that FAPs derived from the mdx 4cv mice, a murine model of Duchenne muscular dystrophy, display a heightened migratory phenotype due to enhanced LPA signaling compared to wild-type FAPs. Remarkably, we found that the inhibition of LPA 1 or YAP transcriptional coactivator activity in mdx 4cv FAPs reverts this phenotype. In summary, the identified LPA-LPA 1 -YAP pathway emerges as a critical driver of skeletal muscle FAPs migration and provides insights into potential novel targets to mitigate fibrosis in muscular dystrophies. [ABSTRACT FROM AUTHOR]

Irritability and attention-deficit/hyperactivity disorder (ADHD) symptoms frequently co-occur in youth. Although ADHD has been associated with inhibitory control deficits, the literature on irritability and inhibitory control is mixed. Examining how irritability, ADHD symptoms, and inhibitory control interrelate both cross-sectionally and longitudinally across development could shed light on common and distinct mechanisms of youth psychopathology. We utilized a cross-lagged panel model with data from 2 time points (at ages 10 and 12 years) of the Adolescent Brain and Cognitive Development (ABCD) Study (N = 7,444, or ∼63% of the baseline sample with full data at each time point) to test cross-sectional and longitudinal associations among parent-reported irritability and ADHD symptoms and behaviorally assessed inhibitory control. This was performed separately across discovery and replication subsamples, each n = 3,722. As expected, irritability and ADHD symptoms exhibited strong cross-sectional and reciprocal cross-lagged associations. Higher ADHD symptoms at age 10 years were associated concurrently with poorer inhibitory control and predicted poorer inhibitory control at age 12. Contrary to predictions, inhibitory control was not significantly associated with irritability cross-sectionally, nor was it predictive of later irritability or ADHD symptoms. These findings highlight strong links between irritability and ADHD. Although inhibitory control deficits were linked to ADHD and predictive of its symptom course, inhibitory control had no significant associations with irritability. Future research should investigate other candidate mechanisms of the co-occurrence of irritability and ADHD symptoms and predictors of their developmental trajectories. This study investigated how irritability, ADHD symptoms, and inhibitory control interrelate both cross-sectionally and longitudinally in a sample of youth from the Adolescent Brain and Cognitive Development (ABCD) Study (N = 7,444). Results indicate that irritability and ADHD symptoms exhibit strong reciprocal predictive relationships; however, inhibitory control does not predict later irritability or ADHD, though ADHD symptoms predicted later inhibitory control deficits. These findings corroborate the predictive relations between irritability and ADHD over development and highlight the need for continued exploration of mechanisms underlying their co-occurrence. [ABSTRACT FROM AUTHOR]

Cognitive impairments affect functional capacity in individuals with schizophrenia (SZH), but their neural basis remains unclear. The Wisconsin Card Sorting Test (WCST), and the Stroop Task (SCWT), are paradigmatic tests which have been used extensively for examining executive function in SZH. However, few studies have explored how deficits on these tasks link to brain volume differences commonly seen in SZH. Here, for the first time, we tested associations between FreeSurfer-derived frontal brain volumes and performance on both WCST and SCWT, in a well-matched sample of 57 SZH and 32 control subjects. We also explored whether these associations were dissociable from links to symptom severity in SZH. Results revealed correlations between volumes and task performance which were unique to SZH. In SZH only, volumes of right middle frontal regions correlated with both WCST and Stroop performance: correlation coefficients were significantly different to those present in the control group, highlighting their specificity to the patient group. In the Stroop task, superior frontal regions also showed associations with Stroop interference scores which were unique to SZH. These findings provide important detail around how deficits on these two paradigmatic executive function tasks link to brain structural differences in SZH. Results align with converging evidence suggesting that neuropathology within right middle frontal regions (BA9 and BA46) might be of particular import in SZH. No volumetric associations with symptom severity were found, supporting the notion that the structural abnormalities underpinning cognitive deficits in SZH differ from those associated with symptomatology. [ABSTRACT FROM AUTHOR]

Depression and obesity are associated with impaired inhibitory control. Behavioral evidence indicates an exacerbating additive effect when both conditions co-occur. However, the underlying neural mechanisms remain unclear. Moreover, systemic inflammation affects neurocognitive performance in both individuals with depression and obesity. Here, we investigate additive effects of depression and obesity on neural correlates of inhibitory control, and examine inflammation as a connecting pathway. We assessed inhibitory control processing in 64 individuals with obesity and varying degrees of depressed mood by probing neural activation and connectivity during an fMRI Stroop task. Additionally, we explored associations of altered neural responses with individual differences in systemic inflammation. Data were collected as part of the BARICO (Bariatric surgery Rijnstate and Radboudumc neuroimaging and Cognition in Obesity) study. Concurrent depression and obesity were linked to increased functional connectivity between the supplementary motor area and precuneus and between the inferior occipital and inferior parietal gyrus. Exploratory analysis revealed that circulating inflammation markers, including plasma leptin, IL-6, IL-8, and CCL-3 correlated with the additive effect of depression and obesity on altered functional connectivity. The observational design limits causal inferences. Future research employing longitudinal or intervention designs is required to validate these findings and elucidate causal pathways. These findings suggest increased neural crosstalk underlying impaired inhibitory control in individuals with concurrent obesity and depressed mood. Our results support a model of an additive detrimental effect of concurrent depression and obesity on neurocognitive functioning, with a possible role of inflammation. • Depression and obesity are both associated with impaired inhibitory control. • We studied the neurocognitive effects of co-occurring obesity and depression. • Co-occurrence of both conditions was related to increased fMRI neural crosstalk. • Inflammation markers correlated with connectivity changes in depression and obesity. • Findings support a model of additive detrimental effects on inhibitory control. [ABSTRACT FROM AUTHOR]

Stress in surgeons is well-known for its negative impact on neurocognition and surgical performance. Surgeons commonly use music for stress reduction, but its specific effects on neurosurgeons remain unclear. This study aims to investigate how listening to music during microsurgery affects neurocognitive (NC) functions, subjective anxiety, and stress levels in neurosurgeons. Conducted in 2 phases, the pilot phase involved 23 neurosurgeons completing a survey and rating compositions based on ragas of North Indian/Hindustani classical music for suitability during surgery. Five excerpts were selected for the main phase, which involved 3 neurosurgeons performing 16 surgeries, 8 with and 8 without music. Data collection included presurgery assessments of sleep, caffeine intake, subjective stress levels, perceived complexity of the surgery that was to be performed, and NC tasks. Postsurgery subjective stress levels, actual complexity, and surgeon experiences with music were recorded. While there was a trend toward reduced stress and perceived complexity with music, statistical significance was not reached. NC tasks showed nonsignificant improvement with music, with a significant (at P < 0.001) speed-accuracy trade-off noted in response inhibition. Music appears to reduce subjective stress and task complexity, influencing neurocognition, particularly through speed-accuracy trade-offs. Further research is needed to understand its mechanisms and appropriate contexts for use before widespread recommendation. [ABSTRACT FROM AUTHOR]

In the current study, it was aimed to evaluate neurotrophic factor levels and their relationship with executive functions in high-risk children and adolescents (high-risk group) whose parents were diagnosed with bipolar disorder (BD) but not affected by any psychiatric disease,and in order to determine possible vulnerability factors related to the disease. The study sample consisted of 32 high-risk group and 34 healthy controls. The Schedule for Affective Disorders and Schizophrenia for School-Age Children-Present and Lifetime Version-Turkish Adaptation (KSADS-PL-T), Stroop Test, Serial Digit Learning Test (SDLT) and Cancellation Test to evaluate executive functions were administered to all participants by the clinician.Serum levels of neurotrophic factors were measured using commercial enzyme linked immunosorbent assay kits. Serum BDNF, NT-3, NT-4 levels and SDLT scores were significantly lower in the high-risk group for BD compared to the healthy control group. A moderate negative correlation was found between BDNF levels and the Cancellation Test scores in the high-risk group. In addition to these results, the odds ratios of age, NT-4, SDLT scores for being in the risky group in terms of BD diagnosis were 1.26, 0.99 and 0.86 respectively. This was a cross-sectional study. Causality between study results is therefore difficult to establish. The relatively small sample size of the study is another limitation. The results of the present study suggest that BDNF, NT-3, NT-4 may play a role in the physiopathology of BD and may be associated with impaired executive function areas such as attention and response inhibition in the high-risk group. • Neurotrophic factors may play a role in the pathophysiology of bipolar disorder. • Neurotrophic factors may be associated with impaired executive functions. • Examination of the offspring of bipolar parents provides an opportunity to investigate early changes. [ABSTRACT FROM AUTHOR]

Diabetes mellitus (DM) is frequently associated with the occurrence and development of depression, and the co-occurrence of diabetes mellitus with depression (DD) may further reduce patients' quality of life. Recent research indicates that dopamine receptors (DRs) play a crucial role in immune and metabolic regulation. Pramipexole (PPX), a D2/3R agonist, has demonstrated promising neuroprotective and immunomodulatory effects. Nevertheless, the therapeutic effects and mechanisms of action of PPX on DM-induced depression are not clear at present. Depression, DM, and DD were induced in a rat model through a combination of a high-fat diet (HFD) supplemented with streptozotocin (STZ) and chronic unpredictable mild stress (CUMS) combined with solitary cage rearing. The pathogenesis of DD and the neuroprotective effects of DRs agonists were investigated using behavioral assays, enzyme-linked immunosorbent assay (ELISA), hematoxylin-eosin (HE) staining, Nissl staining, Western blotting (WB) and immunofluorescence (IF). DD rats exhibited more severe dopaminergic, neuroinflammatory, and neuroplastic impairments and more pronounced depressive behaviors than rats with depression alone or DM. Our findings suggest that DRs agonists have significant therapeutic effects on DD rats and that PPX improved neuroplasticity and decreased neuroinflammation in the hippocampus of DD rats while also promoting DG cell growth and differentiation, ultimately mitigating depression-like behaviors. Our study is based on a rat model. Further evidence is needed to determine whether the therapeutic effects of PPX apply to patients suffering from DD. Neuroinflammation mediated by damage to the dopaminergic system is one of the key pathogenic mechanisms of DD. We provide evidence that PPX has a neuroprotective effect on the hippocampus in DD rats and the mechanism may involve the inhibition of NOD-, LRR- and pyrin domain-containing protein 3 (NLRP3) inflammasome activation by DRs to attenuate the neuroinflammatory response and neuroplasticity damage. [Display omitted] • We have shown experimentally that pramipexole has neuroinflammatory and neuroplasticity-improving effects. This effect has not yet been demonstrated in diabetes mellitus with depression. • Our study found that impairment of the dopaminergic system may exacerbate neuroinflammatory damage in diabetes mellitus with depression. This is likely one of the key causative mechanisms of diabetes mellitus with depression. • Our study showed that pramipexole administration not only improved depressive symptoms, but also ameliorated diabetes mellitus blood glucose disturbances in DD rats. [ABSTRACT FROM AUTHOR]

Hepatic encephalopathy (HE) is a frequent complication of cirrhosis, leading to preventable hospitalizations and increased mortality. Despite the availability of validated neuro-psychometric tests to diagnose HE, only 10% of clinicians regularly screen for HE due to lack of time, equipment, and trained personnel. We studied the association between patient-reported cognitive function and the National Institutes of Health Toolbox Cognition Battery (a validated measure of HE) in patients with cirrhosis. A single-center prospective study of adult patients undergoing liver transplantation evaluation was performed from 10/2020 to 12/2021. Cognition was assessed using the National Institutes of Health Toolbox Cognition Battery and a brief Patient-Reported Outcomes Measurement Information System (PROMIS) survey. Twenty-three liver transplantation candidates were enrolled; the mean age was 56.4 (±9.7) years, 39% were female and the most common etiologies of cirrhosis were primary biliary cirrhosis/primary sclerosing cholangitis/overlap syndrome (30%), hepatitis C (22%) and alcohol-associated liver disease (22%). The mean MELD-Na was 14.9 (±6.4). The mean PROMIS Cognitive Function T-score (PROMIS CF) was 49.2 (±9.6). The mean T-scores for the List Sort Working Memory test, Flanker Inhibitory Control and Attention test, and Pattern Comparison Processing Speed test were 46.4 (±9.9), 37.8 (±6.2), and 50.22 (±16.4), respectively. PROMIS CF correlated with the List Sort Working Memory test (r = 0.45, P =.03). The mean hospitalization rate was 1.6 days admitted per month. On adjusted multivariate analysis, PROMIS CF predicted total hospitalization days (P <.001), hospital admissions (P =.01), and hospitalization rate (P <.001). A brief survey can screen for HE and predict hospitalizations in patients with cirrhosis. [ABSTRACT FROM AUTHOR]

The prevalence of Major Depressive Disorder (MDD) is twice as high in women as in men and this difference already emerges during adolescence. Because the mechanisms underlying this sex-difference remain poorly understood, we took a bottom-up approach to identify factors explaining the sex-MDD relationship. Data came from the TRacking Adolescents' Individual Lives Survey (TRAILS), a population study investigating youths' development from age 11 into adulthood. We assessed multiple baseline covariates (e.g., demographic, social and psychological) at ages 11–13 years and MDD onset at ages 19 and 25 years. In regression analyses, each covariate's role in the sex-MDD association as an effect modifier or confounder/explanatory variable was investigated. Replicability was evaluated in an independent sample. The analyses identified no effect-modifiers. Baseline internalizing problems, behavioral inhibition, dizziness, comfort in classroom, physical complaints, attention problems, cooperation, self/effortful control, interpersonal life events and computer use partially explained the association between sex and MDD at age 19. The association between sex and MDD at age 25 was explained by largely the same variables, but also by shyness, acne, antisocial behavior, aggression, affection from peers and time spent shopping. The explanatory roles of internalizing problems, behavioral inhibition, negative events involving gossip/rumors and leisure-time spending (computer-use/shopping) were replicated. Potentially important baseline variables were not included or had low response rates. Gender roles or identification were not considered. Baseline MDD was not adjusted for. The sex-MDD association is partially explained by sex differences in symptoms and vulnerability factors already present in early adolescence. • Girls have a higher risk of later MDD than boys, but it is unclear why. • Possible explanatory factors (>200) for this sex-MDD association were explored. • Results indicated that girls have increased MDD-vulnerability at an early age. • Aged 11–13, girls already report more mental and somatic symptoms than boys. • No evidence was found for sex-specific MDD-risk mechanisms (effect-modifiers). [ABSTRACT FROM AUTHOR]

The rostral ventromedial medulla (RVM) is the key output node of the descending pain-modulating system. Intrinsic and extrinsic factors contribute to the pain experience by influencing the activity of two functional types of RVM neurons, OFF-cells and ON-cells, which respectively exert inhibitory and facilitatory control over nociceptive transmission and pain. Dysfunction in descending control, which alters the distinct inhibitory and facilitatory outputs of RVM, contributes to persistent pain states. Characterizing the function(s) of genetically defined RVM populations has been challenging and conflicting results have emerged, stressing the need for rigorous interpretation of experiments based on candidate molecular markers. Further investigation of interactions within and between functional RVM populations are a critical next step in improving our understanding of descending control of pain. The descending-pain modulating circuit controls the experience of pain by modulating transmission of sensory signals through the dorsal horn. This circuit's key output node, the rostral ventromedial medulla (RVM), integrates 'top-down' and 'bottom-up' inputs that regulate functionally defined RVM cell types, 'OFF-cells' and 'ON-cells', which respectively suppress or facilitate pain-related sensory processing. While recent advances have sought molecular definition of RVM cell types, conflicting behavioral findings highlight challenges involved in aligning functional and molecularly defined types. This review summarizes current understanding, derived primarily from rodent studies but with corroborating evidence from human imaging, of the role of RVM populations in pain modulation and persistent pain states and explores recent advances outlining inputs to, and outputs from, RVM pain-modulating neurons. [ABSTRACT FROM AUTHOR]

• RMTg lesions reduce LHb induced inhibition of DA firing. • RMTg lesions reduce foot shock induced inhibition of DA firing. • Lower prevalence of neurons with rebound excitation after RMTg lesion. • RMTg lesions increase LHb induced excitation of DA firing. • Low correspondence between foot shock and LHb stimulation response. Dopamine (DA) neurons of the substantia nigra (SN) and ventral tegmental area generally respond to aversive stimuli or the absence of expected rewards with transient inhibition of firing rates, which can be recapitulated with activation of the lateral habenula (LHb) and eliminated by lesioning the intermediating rostromedial tegmental nucleus (RMTg). However, a minority of DA neurons respond to aversive stimuli, such as foot shock, with a transient increase in firing rate, an outcome that rarely occurs with LHb stimulation. The degree to which individual neurons respond to these two stimulation modalities with the same response phenotype and the role of the RMTg is not known. Here, we record responses from single SN DA neurons to alternating activation of the LHb and foot shock in male rats. Lesions of the RMTg resulted in a shift away from inhibition to no response during both foot shock and LHb stimulation. Furthermore, lesions unmasked an excitatory response during LHb stimulation. The response correspondence within the same neuron between the two activation sources was no different from chance in sham controls, suggesting that external inputs rather than intrinsic DA neuronal properties are more important to response outcome. These findings contribute to a literature that shows a complex neurocircuitry underlies the regulation of DA activity and, by extension, behaviors related to learning, anhedonia, and cognition. [ABSTRACT FROM AUTHOR]

The aim of this study was to investigate the differences between resting and active thalamic neurometabolite levels and inhibitory function in obsessive compulsive disorder (OCD) patients with poor sleep quality (PSQ was defined as Pittsburgh Sleep Quality Index >5 and sleep efficiency ≤85%) compared to OCD patients with good sleep quality (GSQ) and healthy controls (HCs), as well as the relationship of these indices to obsessive compulsive symptoms. Functional magnetic resonance spectroscopy (fMRS) was used to measure resting and active thalamic neurometabolite levels in 72 subjects (20 HCs and 38 OCD patients included in study analysis). Response inhibition function was measured by the Go-Nogo task before and during MRS recording. Subjective sleep quality was assessed using the Pittsburgh Sleep Quality Index (PSQI). The symptoms of OCD, anxiety and depression were evaluated using relevant clinical scales. OCD patients exhibited significantly reduced Glx/Cr levels in the resting thalamus. The levels of resting thalamic Glu/Cr and Glx/Cr in OCD patients with PSQ were significantly lowest. OCD patients had significantly lower correct rates on Go tasks, higher error rates on Nogo tasks, and longer error average response times (EART) to the Nogo task. OCD patients with PSQ demonstrated the highest Nogo task error rate and the longest EART to Nogo task. Furthermore, PSQI scores exhibited negative correlations with Glu/Cr and Glx/Cr in the resting thalamus. OCD patients with PSQ demonstrated reduced levels of thalamic resting Glx and more pronounced response inhibitory function impairment. Aberrant neurometabolite levels in critical brain regions, coupled with heightened response inhibition function deficits, may be a neurobiological basis for the PSQ that OCD patients generally exhibit. [ABSTRACT FROM AUTHOR]

Neural analyses of response inhibition rely on separating trials with and without a behavioral response. Can researchers be sure the absence of a behavioral outcome equates to the presence of inhibitory control? We emphasize advancing response inhibition research by utilizing peripheral measures of response progress to define behavioral stopping contrasts. [ABSTRACT FROM AUTHOR]

Response inhibition is a key neurocognitive factor contributing to impulsivity in mood disorders. Here, we explored the common and differential alterations of neural circuits associated with response inhibition in bipolar disorder (BD) and unipolar disorder (UD) and whether the oscillatory signatures can be used as early biomarkers in BD. 39 patients with BD, 36 patients with UD, 29 patients initially diagnosed with UD who later underwent diagnostic conversion to BD, and 36 healthy controls performed a Go/No-Go task during MEG scanning. We carried out time-frequency and connectivity analysis on MEG data. Further, we performed machine learning using oscillatory features as input to identify bipolar from unipolar depression at the early clinical stage. Compared to healthy controls, patients had reduced rIFG-to-pre-SMA connectivity and delayed activity of rIFG. Among patients, lower beta power and higher peak frequency were observed in BD patients than in UD patients. These changes enabled accurate classification between BD and UD with an accuracy of approximately 80 %. The inefficiency of the prefrontal control network is a shared mechanism in mood disorders, while the abnormal activity of rIFG is more specific to BD. Neuronal responses during response inhibition could serve as a diagnostic biomarker for BD in early stage. • The inefficiency of the prefrontal control network is a shared in UD and BD. • The abnormal activity of rIFG is more special to BD. • Beta oscillations during response inhibition could serve as a diagnostic biomarker for BD in early stage. [ABSTRACT FROM AUTHOR]

Response inhibition is a core cognitive impairment in bipolar disorder (BD), leading to increased impulsivity in BD. However, the relationship between the neural mechanisms underlying impaired response inhibition and impulsivity in BD is not yet clear. Individuals who are genetically predisposed to BD give a way of identifying potential endophenotypes. A total of 97 participants, including 39 patients with BD, 22 unaffected relatives (UR) of patients with BD, and 36 healthy controls performed a Go/No-Go task during magnetoencephalography. We carried out time-frequency and connectivity analysis on MEG data. Decreased beta power, prolonged latency and increased peak frequency in rIFG, decreased beta power in pre-SMA and reduced rIFG-to-pre-SMA connectivity were found in BD relative to healthy controls. In the UR group, we found a decrease in the beta power of pre-SMA and prolonged latency of rIFG. Furthermore, increased motor impulsiveness in BD was related to abnormal alterations in beta oscillatory activity of rIFG and functional connectivity between rIFG and pre-SMA. Hypoactivity activity in rIFG and impaired dominant role of rIFG in the prefrontal control network may underlie the neuropathology of response inhibition dysfunction, resulting increased motor impulsivity in BD. Our findings point to measuring rIFG dysfunction as a potential means of identifying individuals at genetic high risk for transition to BD disease expression. • Reduced pre-SMA activation and prolonged rIFG activation relate to genetic risk of BD. • Blunted activation in rIFG and attenuated connectivity from rIFG to pre-SMA reflect disease expression for BD. • Hypofunction in rIFG and disconnectivity with pre-SMA during response inhibition are associated with motor impulsivity in BD. [ABSTRACT FROM AUTHOR]

Anxiety disorders often emerge in adolescence and are associated with risk aversion. Risk aversion conflicts with the typical adolescent approach-motivated phenotype and can interfere with learning and contribute to symptom maintenance. We investigated the neural and behavioral correlates of risk avoidance in a diverse sample of adolescents (N = 137; M Age = 11.3; 34.3 % white, 22.1 % Latino, 20 % Asian, 14.3 % Black, 9.3 % Mixed Race) as they completed a task involving risky decision-making and response inhibition during fMRI. Voluntary cautious choice was compared to successful response inhibition to isolate the neural systems underlying the decision to avoid a risk and identify their relation to risk-taking and anxiety in adolescents. Anxious adolescents self-reported more avoidance but demonstrated normative risk-taking on the laboratory task. Interestingly, they responded quickly during response inhibition but took longer to decide in the face of risk. All youth showed widespread recruitment of decision-making and salience network regions when deciding to avoid risk. The neural mechanisms driving avoidance differed based on anxiety such that left inferior frontal gyrus (IFG) activation was linked to risk avoidance in adolescents with low anxiety and risk-taking in anxious adolescents, while striatal connectivity was linked to risk avoidance in anxious adolescents and risk-taking in those with low anxiety. This work is cross-sectional and therefore cannot speak to causality or directionality of effects. These results suggest that the neural mechanisms contributing to adolescent risk-taking may function to promote avoidance in anxious youth, increasing vulnerability to maladaptive avoidance and further anxiety development. • We examined risk avoidance in 137 early adolescents with varying anxiety severity. • Anxious adolescents inhibited quickly to avoid harm but took longer to avoid risk. • Avoidance was linked to high frontal and low striatal response in low anxiety. • Avoidance was linked to low frontal and high striatal response in high anxiety. • Fronto-striatal mechanisms may promote avoidance in anxious adolescents. [ABSTRACT FROM AUTHOR]

It is not clear whether and how insomnia disorder (ID) impairs response inhibition ability. Fronto-striatal functional connectivity (FC) plays a critical role in response inhibition and is found be abnormal in patients with ID. In this study, we examined whether insomnia symptoms impair response inhibition in a large non-clinical sample and whether impaired response inhibition is related to abnormal fronto-striatal FC. One hundred and fifteen young ID patients and 160 age and sex-matched healthy controls (HC) underwent resting-state functional magnetic response imaging scans and performed the stop-signal task (SST). Performance of SST, Gray Matter Volumes (GMVs), and connections of brain regions related to fronto-striatal circuits was compared between groups. Further examined the association between response inhibition impairment and fronto-striatal FC. The behavioral results showed that patients with ID had significantly longer stop-signal reaction time (SSRT) compared with the HC, reflecting the impaired response inhibition among IDs. Brain imaging results showed IDs had decreased GMVs of the Right Superior Frontal (SFG) and left Supplementary Motor area (SMA). Seed-based FC results showed that compared to HC, the ID showed decreased FC between left SMA and left Paracentral lobule, left SMA and right SMA, and right SFG and right Orbital Middle Frontal gyrus, and increased FC between right SFG and right putamen. Meanwhile, the FC between right SFG and putamen was positively correlated with SSRT in IDs. The current study found significantly impaired response inhibition among ID and this impairment may be related to abnormal fronto-striatal FC in ID. [ABSTRACT FROM AUTHOR]

Inhibitory control is a fundamental mechanism for adaptive behavior and cognition that features in theories across psychology and cognitive science. Although inhibitory control is thought to regulate processes ranging from actions to memories, most neuroscientific work studies these domains of inhibition separately. Recent crossdomain comparisons have converged on the view that inhibitory control arises from common, domain-general neural mechanisms. We propose that an input inhibition mechanism, acting via fronto-subthalamic inhibitory pathways may contribute to domain-general inhibitory control by suppressing thalamic drive of cortical activity. We argue that β-band activity in local circuits constitutes a potential domain-general signature of inhibitory control. Inhibitory control is a fundamental mechanism underlying flexible behavior and features in theories across many areas of cognitive and psychological science. However, whereas many theories implicitly or explicitly assume that inhibitory control is a domain-general process, the vast majority of neuroscientific work has hitherto focused on individual domains, such as motor, mnemonic, or attentional inhibition. Here, we attempt to close this gap by highlighting recent work that demonstrates shared neuroanatomical and neurophysiological signatures of inhibitory control across domains. We propose that the regulation of thalamocortical drive by a fronto-subthalamic mechanism operating in the β band might be a domain-general mechanism for inhibitory control in the human brain. Inhibitory control is a fundamental mechanism underlying flexible behavior and features in theories across many areas of cognitive and psychological science. However, whereas many theories implicitly or explicitly assume that inhibitory control is a domain-general process, the vast majority of neuroscientific work has hitherto focused on individual domains, such as motor, mnemonic, or attentional inhibition. Here, we attempt to close this gap between by highlighting recent work that demonstrates shared neuroanatomical and neurophysiological signatures of inhibitory control across domains. We propose that the regulation of thalamocortical drive by a fronto-subthalamic mechanism operating in the β band might be a domain-general mechanism for inhibitory control in the human brain. [ABSTRACT FROM AUTHOR]

The present study investigated neural mechanisms for suppressing a highly automatic balance recovery step. Response inhibition has typically been researched using focal hand reaction tasks performed by seated participants, and this has revealed a neural stopping network including the Inferior Frontal Gyrus (IFG). It is unclear if the same neural networks contribute to suppressing an unwanted balance reaction. Is there greater IFG activation when suppressing an automatic balance recovery step? Functional near-infrared spectroscopy (fNIRS) was used to measure brain activity in 21 young adults as they performed a balance recovery task that demanded rapid step suppression following postural perturbation. The hypothesis was that the IFG would show heightened activity when suppressing an automatic balance recovery step. A lean and-release system was used to impose temporally unpredictable forward perturbations by releasing participants from a supported forward lean. For most trials (80%), participants were told to recover balance by quickly stepping forward (STEP). However, on 20% of trials at random, a high-pitch tone was played immediately after postural perturbation signaling participants to suppress a step and fully relax into a catch harness (STOP). This allowed us to target the ability to cancel an already initiated step in a balance recovery context. Average oxygenated hemoglobin changes were contrasted between STEP and STOP trials, 1–6 s post perturbation. The results showed a greater bilateral prefrontal response during STOP trials, supporting the idea that executive brain networks are active when suppressing a balance recovery step. Our study demonstrates one way in which higher brain processes may help us prevent falls in complex environments where behavioral flexibility is necessary. This study also presents a novel method for assessing response inhibition in an upright postural context where rapid stepping reactions are required. • Functional near infrared spectroscopy measured brain activation in a balance task. • Automatic step reactions were occasionally interrupted by a stop cue. • Prefrontal cortical activity increased when suppressing a balance recovery step. • This demonstrates a novel way to probe inhibition in a reactive balance task. [ABSTRACT FROM AUTHOR]

• We studied saccade performance to study the underlying basal ganglia (BG) pathophysiology in Segawa's disease (SD). • We found a mild delay in latency of memory guided saccades and impairment to suppress reflexive saccades in SD. • Dopamine deficiency manifests in oculomotor abnormalities during development with delayed maturation especially in male patients. Objective: To investigate the oculomotor manifestations of Segawa disease (SD), considered to represent mild dopamine deficiency and discuss their pathophysiological basis. Methods: We recorded visually- (VGS) and memory-guided saccade (MGS) tasks in 31 SD patients and 153 age-matched control subjects to study how basal ganglia (BG) dysfunction in SD evolves with age for male and female subjects. Results: SD patients were impaired in initiating MGS, showing longer latencies with occasional failure. Patients showed impaired ability to suppress reflexive saccades; saccades to cues presented in MGS were more frequent and showed a shorter latency than in control subjects. These findings were more prominent in male patients, particularly between 13 and 25 years. Additionally, male patients showed larger delay in MGS latency in trials preceded by saccades to cue than those unpreceded. Conclusions: The findings can be explained by a dysfunction of the BG-direct pathway impinging on superior colliculus (SC) due to dopamine deficiency. The disturbed inhibitory control of saccades may be explained by increased SC responsivity to visual stimuli. Significance: Oculomotor abnormalities in SD can be explained by dysfunction of the BG inhibitory pathways reaching SC, with a delayed maturation in male SD patients, consistent with previous pathological/physiological studies. [ABSTRACT FROM AUTHOR]

Adolescence is a unique period of psychosocial growth during which social adversity can negatively influence mental health trajectories. Understanding how adolescent social stress impacts males and females and why some individuals are particularly affected is becoming increasingly urgent. Social defeat stress models for adolescent male mice have been effective in reproducing some physical/psychological aspects of bullying. Designing a model suitable for females has proven challenging. We report a version of the adolescent male accelerated social defeat stress (AcSD) paradigm adapted for females. Early adolescent C57BL/6J female mice (N = 107) were exposed to our modified AcSD procedure twice a day for 4 days and categorized as resilient or susceptible based on a social interaction test 24 hours later. Mice were then assessed for changes in Netrin-1/DCC guidance cue expression in dopamine systems, for inhibitory control in adulthood using the Go/No-Go task, or for alterations in dopamine connectivity organization in the matured prefrontal cortex. Most adolescent females showed protection against stress-induced social avoidance, but in adulthood, these resilient females developed inhibitory control deficits and showed diminution of prefrontal cortex presynaptic dopamine sites. Female mice classified as susceptible were protected against cognitive and dopaminergic alterations. AcSD did not alter Netrin-1/DCC in early adolescent females, contrary to previous findings with males. Preserving prosocial behavior in adolescent females may be important for survival advantage but seems to come at the price of developing persistent cognitive and dopamine deficiencies. The female AcSD paradigm produced findings comparable to those found in males, allowing mechanistic investigation in both sexes. [ABSTRACT FROM AUTHOR]

Prior evidence has linked inflammation with impulsivity, but most of this evidence is cross-sectional. In this study, we provoked an acute inflammatory cytokine response to see whether it lowered prepotent response inhibition on three cognitive tasks. This study features secondary analyses from a randomized crossover trial in which 171 postmenopausal breast cancer survivors (Stage I-IIIA) each received a typhoid capsular polysaccharide vaccination and a saline placebo injection in a random sequence at two separate visits at least one month apart. Participants completed the Stroop Color-Discrepant Task, the 2-back, and the Conners Continuous Performance Test (CPT) on the computer between 5 and 7 h after the injections. They had their blood drawn once before and repeatedly after the injection to measure interleukin-1 receptor antagonist and interleukin-6 responses. Women committed marginally fewer errors on the Stroop color-discrepant trials after the typhoid vaccine (M = 0.36, SE = 0.08), compared to placebo (M = 0.54, SE = 0.09, p =.076). Injection type did not predict 2-back accuracy (p =.80) or CPT commission errors (p =.47). Inflammatory cytokine responses were also unrelated to the outcomes of interest (p s>.16). We found no evidence that an acute inflammatory cytokine response provokes response disinhibition – an important facet of impulsivity. In fact, our only marginally non-significant result suggested that women were better able to inhibit their prepotent responses on the Stroop after receiving the typhoid vaccine, compared to placebo. Further experimental tests of the acute inflammatory cytokine response's effect on other aspects of impulsivity are warranted. The sample was female, primarily White, highly educated cancer survivors, and recruitment was not premised on impulsive traits or diagnosis with an impulsive-related disorder. Also, there are many facets of impulsivity, and this study only measured response inhibition. • Whether inflammation drives impulsivity or impulsive-related disorders is unclear. • We manipulated inflammation and measured response inhibition among 171 women. • They had a typhoid vaccine and placebo injection in a random order at two visits. • We found no evidence that acute inflammation provoked response disinhibition. • Further research should see if inflammation affects other aspects of impulsivity. [ABSTRACT FROM AUTHOR]

• No response accuracy costs related to increasing cognitive load during walking. • No response speed costs related to increasing cognitive load during walking. • No gait consistency costs related to increasing cognitive load during walking. • Increasing cognitive load during walking came with widespread EEG changes. This study elucidates the neural mechanisms underlying increasing cognitive load while walking by employing 2 versions of a response inhibition task, the '1-back' version and the more cognitively demanding '2-back' version. By using the Mobile Brain/Body Imaging (MoBI) modality, electroencephalographic (EEG) activity, three-dimensional (3D) gait kinematics and task-related behavioral responses were collected while young adults (n = 61) performed either the 1-back or 2-back response inhibition task. Interestingly, increasing inhibitory difficulty from 1-back to 2-back during walking was not associated with any detectable costs in response accuracy, response speed, or gait consistency. However, the more difficult cognitive task was associated with distinct EEG component changes during both successful inhibitions (correct rejections) and successful executions (hits) of the motor response. During correct rejections, ERP changes were found over frontal regions, during latencies related to sensory gain control, conflict monitoring and working memory storage and processing. During hits, ERP changes were found over left-parietal regions during latencies related to orienting attention and subsequent selection and execution of the motor plan. The pattern of attenuation in walking-related EEG amplitude changes, during 2-back task performance, is thought to reflect more effortful recalibration of neural processes, a mechanism which might be a key driver of performance maintenance in the face of increased cognitive demands while walking. Overall, the present findings shed light on the extent of the neurocognitive capacity of young adults and may lead to a better understanding of how factors such as aging or neurological disorders could impinge on this capacity. [ABSTRACT FROM AUTHOR]

Facilitating communication between generations has become increasingly important. However, individuals often demonstrate a preference for their own age group, which can impact social interactions, and such bias in young adults even extends to inhibitory control. To assess whether older adults also experience this phenomenon, a group of younger and older adults completed a Go/NoGo task incorporating young and old faces, while undergoing functional magnetic resonance imaging. Within the networks subserving successful and unsuccessful response inhibition, patterns of activity demonstrated distinct neural age bias effects in each age group. During successful inhibition, the older adult group demonstrated significantly increased activity to other-age faces, whereas unsuccessful inhibition in the younger group produced significantly enhanced activity to other-age faces. Consequently, the findings of the study confirm that neural responses to successful and unsuccessful inhibition can be contingent on the stimulus-specific attribute of age in both younger and older adults. These findings have important implications in regard to minimizing the emergence of negative consequences, such as ageism, as a result of related implicit biases. [ABSTRACT FROM AUTHOR]

Suicidal thoughts and behaviors (STBs) in elementary school-aged youth have increased in recent years. Understanding the risks associated with childhood STBs is necessary for prevention efforts. The current study examined clinical and neurocognitive characteristics of a community sample of elementary school-aged children with (STB+) and without (STB-) a history of STBs. The final sample included 93 families with children average age of 7.8 years (SD = 1.3). Children in this sample were racially diverse, evenly split by sex, and most identified as non-Hispanic. Neurocognitive functioning was assessed using computerized behavioral measures. Child clinical characteristics were assessed using self-report measures and STB history was assessed using semi-structured interviews. Of the 93 families, 64 STB- children and 29 STB+ children participated. On average, STB+ children were older, reported higher levels of depressive and anxiety symptoms, and were more likely to have a parental history of suicidal behavior (PH+). Regarding neurocognitive functioning, STB+ children exhibited lower raw scores for both the NIH Dimensional Change Card Sort Task (NIH-DCCS) and NIH Flanker Inhibitory Control and Attention Test (NIH-Flanker). Multivariable regression analyses revealed raw scores for NIH-DCCS and NIH-Flanker, PH+ status, and child age were associated with childhood STBs. Prospective data is needed to confirm cross-sectional findings. Poorer neurocognitive functioning and PH+ status may serve as risk markers for STBs in elementary school-aged children. Targeting prevention programming for these risks may reduce the likelihood of STBs in at-risk elementary school-aged youth. • Neurocognitive functioning of 6–9-year-old youth with and without a history of STBs • STB+ children exhibited more neurocognitive deficits compared to STB- children. • Parental history of SB, age, and neurocognitive functioning related to child STBs [ABSTRACT FROM AUTHOR]

• The cerebellum may be more involved than previously thought in saccade initiation. • This may be aggravated some time after disease onset. • Cerebellar output defects were associated with a shorter acceleration period and longer deceleration period for saccades. To study how the pathophysiology underlying hereditary spinocerebellar degeneration (spinocerebellar ataxia; SCA) with pure cerebellar manifestation evolves with disease progression using saccade recordings. We recorded visually- (VGS) and memory-guided saccade (MGS) task performance in a homogeneous population of 20 genetically proven SCA patients (12 SCA6 and eight SCA31 patients) and 19 normal controls. For VGS but not MGS, saccade latency and amplitude were increased and more variable than those in normal subjects, which correlated with cerebellar symptom severity assessed using the International Cooperative Ataxia Rating Scale (ICARS). Parameters with significant correlations with cerebellar symptoms showed an aggravation after disease stage progression (ICARS > 50). The saccade velocity profile exhibited shortened acceleration and prolonged deceleration, which also correlated with disease progression. The main sequence relationship between saccade amplitude and peak velocity as well as saccade inhibitory control were preserved. The cerebellum may be involved in initiating VGS, which was aggravated acutely during disease stage progression. Dysfunction associated with disease progression occurs mainly in the cerebellum and brainstem interaction but may also eventually involve cortical saccade processing. Saccade recording can reveal cerebellar pathophysiology underlying SCA with disease progression. [ABSTRACT FROM AUTHOR]

Ample evidence links impaired inhibitory control, attentional distortions, emotional dysregulation, and obsessive-compulsive disorder (OCD). However, it remains unclear what underlies the deficit that triggers the OCD cycle. The present study used an antisaccade paradigm with emotional valences to compare eye movement patterns reflecting inhibitory control and attention switching in OCD and healthy control groups. Thirty-two patients with OCD and thirty healthy controls performed the antisaccade task with neutral, positive, and negative visual images served as fixation stimuli. Presentation of the fixation stimulus overlapped with target stimuli appearance for 200 ms. The OCD group showed more errors to negative stimuli than the control group and they also performed antisaccades more slowly to negative and neutral stimuli than positive ones. Other patterns, including mean gaze velocity of correct antisaccades did not differ between groups. The mean gaze velocity of correct antisaccades was higher for negative and positive stimuli than for neutral stimuli in both groups. The peak velocity parameter did not show any differences either between groups or between valences. The findings support a hypothesis that an attentional bias toward negative stimuli interferes with inhibitory control in OCD. • Increased error rate in response to negative stimuli in antisaccade task in OCD participants; • OCD group made the correct antisaccade in negative and neutral stimuli with longer latency than in positive stimuli; • Both groups made correct antisaccades faster in negative and positive stimuli than in neutral ones. [ABSTRACT FROM AUTHOR]

Joint attention (JA) is fundamental to the development of children's social functioning; both its response and initiation are closely related to executive function (EF), but the relationship between JA and EF has been relatively rarely studied. The present study aimed to investigate the between-condition differences in brain activation and synchronization of JA under four conditions: (1) stranger-Initiating Joint Attention (Stranger-IJA); (2) teacher-Initiating Joint Attention (Teacher-IJA); (3) stranger-Responding to Joint Attention (Stranger-RJA); and (4) teacher-Responding to Joint Attention (Teacher-RJA). It also aimed to explore the relationships between neuroimaging data and children's inhibitory control levels. To address these two goals, the present study employed 41 (aged 58.61 ± 8.64 months, 24 boys) preschool children through behavioral and functional Near-Infrared Spectroscopy (fNIRS) brain imaging assessment to measure children's EF and brain function under JA, respectively. The results revealed that: (1) a significantly higher prefrontal cortex (PFC) activation was triggered in IJA than RJA; (2) a significantly higher brain activation was triggered in JA with a stranger than with a teacher; (3) a significantly higher index of synchronization asymmetry was evoked in the left and right PFC during interaction with the teacher than with the stranger; and (4) preschoolers' brain activation and synchronization were correlated with their inhibitory control level. The findings advance our understanding of preschoolers' social cognitive development with a biological aspect, offer an opportunity to understand the potential risk of the neural disorder in preschoolers, and provide a basis and insight for preventing neural developmental disorders. • Preschoolers revealed higher prefrontal cortex activation in initiating joint attention than in responding to joint attention. • Preschoolers showed higher synchronization asymmetry index in interacting with the teacher than the stranger. • The higher level of inhibitory control, the higher brain synchronization in condition of Teacher-Initiating Joint Attention. [ABSTRACT FROM AUTHOR]

• We investigate effects of different theta/beta neurofeedback (NF) protocols on mechanisms underlying response inhibition in ADHD. • Different NF protocols lead to response inhibition improvements via different neurophysiological mechanisms. • The interactive relationship of theta and beta band activity extends the understanding of oscillatory dynamics in the brain. In attention deficit/hyperactivity disorder (ADHD), impaired response inhibition is frequently observed. A promising non-pharmacological treatment is electroencephalography (EEG)-neurofeedback (NF) training. However, the widely used theta-down/beta-up regulation (↓θ↑β) NF protocol may not be optimal for targeting these deficits. We examined how neurofeedback protocols training the upregulation of theta and/or beta power affect inhibitory control in children and adolescents with ADHD. 64 patients with ADHD took part in the three NF trainings. Aside from parent-reported ADHD symptoms and behavioural performance data, neurophysiological parameters collected via a Go/Nogo task and corrected to account for intraindividual variability were compared in a pre-post design and to an ADHD (n = 20) as well as a typically developing control group (n = 24). The examined NF protocols resulted in similar improvements in response inhibition with the neurophysiological mechanisms differing substantially. The upregulation of theta led to a specific Nogo-P3 increase, while training beta upregulation as well as the combined protocol resulted in less specific effects. This study shows distinct effects of different theta/beta-neurofeedback protocols on the neural mechanisms underlying improvements in response inhibition in patients with ADHD. These effects shed further light on the oscillatory dynamics underlying cognitive control in ADHD and how these may be targeted in neurofeedback treatments. [ABSTRACT FROM AUTHOR]

The taxonomy of autogenous- and reactive-type obsessive-compulsive disorder (OCD) (AO vs. RO) is one of the most valid subtyping approaches to the heterogeneity of OCD. The present study aimed to seek evidence of neural substrates supporting the dissociation of cognition inhibition in AO and RO which was revealed by our previous behavioral and electrophysiological work. A total of 165 patients with OCD (86 AO versus 79 RO), and 79 healthy controls (HC) underwent resting-state functional magnetic resonance imaging scans. Within-network connectivity, node strength, and edge-wise functional connectivity (FC) in cognition and response inhibition networks were calculated. Results from 3 cognition and 2 response inhibition network atlases were compared to confirm the robustness of the findings. Both AO and RO showed lower within-network connectivity in response inhibition networks, while lower within cognition inhibition network connectivity was only detected in AO. Besides shared weaker node strength in the anterior insula (AI), anterior cingulate cortex (ACC), and supplementary motor area (SMA), AO had a broader range of nodes within cognition inhibition networks exhibiting weaker strength, including nodes in right inferior frontal gyrus (IFG), left parietal and occipital regions. Decreased FC of left AI-CC, left IFG-ACC, and frontal-parietal regions in cognition inhibition networks were found in AO. Findings indicate that unlike deficits in connectivity within response inhibition networks which may reflect a common pathology in AO and RO, deficits in connectivity within cognition inhibition networks were more pronounced in AO. These findings strengthen our insight into the heterogeneity in OCD. • Both AO and RO demonstrated lower within response inhibition network connectivity. • Weaker within cognition inhibition network connectivity was only detected in AO. • AO had more nodes within cognition inhibition network exhibiting weaker strength. • Weaker FC between frontoparietal regions within inhibition networks were found in AO. • Findings strengthened our insight into the heterogeneity in OCD. [ABSTRACT FROM AUTHOR]

Depressed individuals are excessively sensitive to negative information but blunt to positive information, which has been considered as vulnerability to depression. Here, we focused on inhibitory control over attentional bias on social evaluation in individuals with depression. We engaged individuals with and without depressive symptoms (categorized by Beck Depression Inventory-II) in a novel attention control task using positive and negative evaluative adjectives as self-referential feedback given by social others. Participants were instructed to look at sudden onset feedback targets (pro-saccade) or the mirror location of the targets (anti-saccade) when correct saccade latencies and saccade errors were collected. The two indices showed that while both groups displayed longer latencies and more errors for anti-saccade relative to pro-saccade responses depressed individuals spent more time reacting correctly and made more errors than non-depressed individuals in the anti-saccade trials and such group differences were not observed in the pro-saccade trials. Although group differences in correct anti-saccade latencies were found for both positive and negative stimuli, depressed individuals spent more time making correct anti-saccade responses to negative social feedback than to positive ones whereas non-depressed individuals featured longer correct anti-saccade latencies for positive relative to negative evaluations. Our results suggest that depressed individuals feature an impaired ability in attention control for self-referential evaluations, notably those of negative valence, shedding new light on depression-distorted self-schema and corresponding social dysfunctions. • Depression-altered inhibitory control over attention to social feedback was examined. • Depressed individuals displayed impaired attention control for negative evaluation. • Non-depressed individuals exhibited reduced inhibition over positive feedback. • The findings contribute to understanding depression-induced social dysfunctions. [ABSTRACT FROM AUTHOR]

Both the Neurovisceral Integration Model and the Vagal Tank Theory propose cardiac vagal activity (CVA) as proxy for self-regulatory or processing resources required for attentional and top-down control as key mechanisms in executive functioning or emotion-regulation. These resources have, according to the Dual Competition Model, limited capacity and are prioritized for processing the most salient of different competing stimuli. As such, emotional and especially negative or threatening stimuli attract these self-regulatory/processing resources, and may thus interfere with ongoing cognitive processes if not integrated adaptively. Here, we investigated whether tonic and phasic CVA represent self-regulatory/processing resources and thus predict response inhibition in an emotional stop-signal task as a measure of cognitive-affective integration. Thereby, we examined not only the independent effects of tonic and phasic CVA, but whether and how the interaction of both variables predicts response inhibition. We assumed that the effects of CVA on response inhibition would be more pronounced in negatively-valenced trials compared to positive or neutral ones. Our results show that CVA significantly predicted response inhibition, with higher tonic CVA predicting faster, and larger phasic withdrawal CVA predicting slower stop-signal reaction times. The interactive effects of tonic and phasic CVA revealed that high tonic CVA levels prevented the negative effects of CVA withdrawal on response inhibition. Contrary to our assumption, we did not find differential effects of tonic and phasic CVA on trials with different valences. Our results support the notion of CVA as index for self-regulatory/processing resources. However, further research is needed to investigate how CVA is related to specific neural processes of cognitive-affective processing. • Higher levels of tonic cardiac vagal activity (CVA) predict better performance in an emotional stop-signal task (ESST) • Phasic withdrawal of CVA impairs ESST performance • Higher levels of tonic CVA prevent the negative effects of phasic withdrawal of CVA on cognitive-affective processing • Phasic increases of CVA can counteract the negative effects of low tonic CVA levels on cognitive-affective processing • Links between tonic and phasic measures of CVA and ESST performance did not differ between stimuli of different valence [ABSTRACT FROM AUTHOR]

Pharmacological ascorbate (P-AscH-; high dose given intravenously) generates H 2 O 2 that is selectively cytotoxic to cancer compared to normal cells. The RAS-RAF-ERK1/2 is a major signaling pathway in cancers carrying RAS mutations and is known to be activated by H 2 O 2. Activated ERK1/2 also phosphorylates the GTPase dynamin-related protein (Drp1), which then stimulates mitochondrial fission. Although early generation of H 2 O 2 leads to cytotoxicity of cancer cells, we hypothesized that sustained increases in H 2 O 2 activate ERK-Drp1 signaling, leading to an adaptive response; inhibition of this pathway would enhance the toxicity of P-AscH-. Increases in phosphorylated ERK and Drp1 induced by P-AscH- were reversed with genetic and pharmacological inhibitors of ERK and Drp1, as well as in cells lacking functional mitochondria. P-AscH- increased Drp1 colocalization to mitochondria, decreased mitochondrial volume, increased disconnected components, and decreased mitochondrial length, suggesting an increase in mitochondrial fission 48 h after treatment with P-AscH-. P-AscH- decreased clonogenic survival; this was enhanced by genetic and pharmacological inhibition of both ERK and Drp1. In murine tumor xenografts, the combination of P-AscH- and pharmacological inhibition of Drp1 increased overall survival. These results suggest that P-AscH- induces sustained changes in mitochondria, through activation of the ERK/Drp1 signaling pathway, an adaptive response. Inhibition of this pathway enhanced the toxicity P-AscH- to cancer cells. [Display omitted] • Increases in phosphorylated ERK and Drp1 induced by pharmacological ascorbate (P-AscH-) were reversed with genetic and pharmacological inhibitors of ERK and Drp1. • Pharmacological ascorbate increased mitochondrial fission after treatment with pharmacological ascorbate. • Pharmacological ascorbate decreased in vitro and in vivo growth which was enhanced by genetic and pharmacological inhibition of both ERK and Drp1. • Pharmacological ascorbate induces sustained increases in mitochondrial oxidative stress and changes in mitochondrial dynamics, through activation of the ERK/Drp1 signaling pathway. [ABSTRACT FROM AUTHOR]

Reversal learning is a crucial aspect of behavioral flexibility that plays a significant role in environmental adaptation and development. While previous studies have established a link between anxiety and impaired reversal learning ability, the underlying mechanisms behind this association remain unclear. This study employed a probabilistic reversal learning task with electroencephalographic recording to investigate these mechanisms. Participants were divided into two groups based on their scores on Spielberger's State-Trait Anxiety Inventory: high trait-anxiety (HTA) and low trait-anxiety (LTA), consisting of 50 individuals in each group. The results showed that the HTA group had poorer reversal learning performance than the LTA group, including a lower tendency to shift to the new optimal option after rule reversals (reversal-shift). The study also examined event-related potentials elicited by reversals and found that although the N1 (related to attention allocation), feedback-related negativity (FRN: related to belief updating), and P3 (related to response inhibition) were all sensitive to the grouping factor, only the FRN elicited by reversal-shift mediated the relationship between anxiety and the number/reaction time of reversal-shift. From these findings, we suggest that abnormalities in belief updating may contribute to the impaired reversal learning performance observed in anxious individuals. In our opinion, this study sheds light on potential targets for interventions aimed at improving behavioral flexibility in anxious individuals. • Higher anxiety is associated with poorer reversal learning performance. • This study aimed to elucidate the underlying electrophysiological mechanisms. • High anxiety subjects showed reduced neuroelectric response during rule reversals. • Feedback-related negativity mediated the association between anxiety and reversals. [ABSTRACT FROM AUTHOR]

Inhibitory control impairment in alcohol use disorder (AUD) may indicate detrimental effects of chronic alcohol use on different functional systems in the brain, but the current studies lack consistency. This study aims to identify the most consistent response inhibition-related brain dysfunction based on existing data. We performed systematic searches of the PubMed, Embase, Web of Science, and PsychINFO databases for available studies. Anisotropic effect-size signed differential mapping was used to quantitatively analyze the differences in response inhibition-related brain activation between AUD patients and HCs. Meta regression was used to explore the relationship between brain alterations and clinical variables. The brain hypoactivation or hyperactivation in AUD patients compared with HCs during the response inhibition tasks was mainly located in the prefrontal cortex including the superior frontal gyrus, inferior frontal gyrus, and middle frontal gyrus, anterior cingulate gyrus (ACC), superior temporal gyrus, occipital gyrus, and somatosensory areas including postcentral gyrus and supramarginal gyrus. The meta-regression revealed that older patients were more likely to present activation in the left superior frontal gyrus when performing the response inhibition tasks. The response inhibitive dysfunctions in a distinct prefrontal-cingulate cortices may presumably reflect the core impairment in cognitive control abilities. Dysfunction in the occipital gyrus and somatosensory areas may indicate an abnormal motor-sensory and visual function in AUD. Such functional abnormalities may represent neurophysiological correlates of the executive deficits observed in AUD patients. This study has been registered in PROSPERO (number CRD42022339384). [ABSTRACT FROM AUTHOR]

Reinforcement sensitivity theory (RST) is proposed as a neurobiological system that eventually led to emotion and motivation-based constructs of personality. Traditionally segmented into the behavioral activation system (BAS) and the behavioral inhibition system (BIS), RST is commonly used to describe personality and behavior. Although there have been studies linking gray matter alterations with BIS/BAS subscales, the role of white matter (WM) alterations is yet controversial. We aimed to investigate the specific WM tracts associated with BIS/BAS scores. 220 healthy participants (mean age = 39.14 ± 20.23, 80 (35.7 %) females) were evaluated using the BIS/BAS questionnaire from the LEMON database. Diffusion MRI connectometry (DMRI) was used to investigate the WM correlates of BIS/BAS subscales in each gender group. Multiple regression models with the covariates of age, handedness, and education were fitted to address the correlation of local connectomes with BIS/BAS components. DMRI connectometry revealed that the quantitative anisotropy (QA) value of the splenium of the corpus callosum, right cerebellum, middle cerebellar peduncle, and superior cerebellar peduncle, had a significant negative correlation with each BIS/BAS subscale. In contrast, the QA value in the body of the corpus callosum and bilateral cingulum showed a positive correlation with BIS/BAS subscales. The integrity of WM in certain tracts is associated with behavioral activation and inhibition. This finding expands our knowledge of the neural networks associated with risk-taking and reward-seeking behaviors. • Brain microstructures are associated with risk-taking and reward-seeking behaviors. • Quantitative anisotropy was correlated with behavioral activation and inhibition. • Future studies are warranted to increase our knowledge of this association. [ABSTRACT FROM AUTHOR]

The goal of the current study was to examine differences in neurocognitive processes across groups marked by binge drinking and depression to identify patterns of cognitive and affective processing impairments. Undergraduate students (N = 104; 64% female) were recruited based on self-reported symptoms of depression and alcohol use. They completed an emotional Go/No-Go task while undergoing EEG. Mean amplitudes for N2 and P3 components were examined with 2 (Depressed/Non-depressed) X 2 (Binge/Non-binge drinkers) X 4 (Happy/Sad/Angry/Calm) X 3 (Left/Middle/Right) X 2 (Go/No-Go) repeated measures ANOVAs. There were significant Trial Type X Valence X Depression X Binge Drinking interactions for N2 (F (3, 80) = 6.62, p <.01) and P3 (F (3, 80) = 4.65, p <.01) components. There was a significant Valence X Depression X Binge Drinking interaction for response bias (F (3, 65) = 3.11, p <.05). The source of our sample may be a limitation, as all participants were university students, potentially making the results less generalizable. Further, we cannot be certain that social desirability did not interfere with honest reporting of alcohol use in this population. Differences in early inhibitory control were observed across emotions based on trial type among depressed non-binge drinkers, and these differences were attenuated in the presence of binge drinking. Further, the effects of depression on later inhibitory control were specific to non-binge drinkers. Results help to clarify the nature of underlying patterns of neurocognitive and affective risk processes that could be targeted by prevention and intervention programs. • In early stages of processing, depressed non-binge drinkers required greater attentional engagements, as evidence by enhanced N2 amplitudes on Go trials. • In early stages of processing, the effects of depression were attenuated among binge drinkers, suggesting that emerging adults may use alcohol to regulate affect. • During later stages of processing, attenuated P3 amplitudes were observed in the context of depressive symptoms and absence of binge drinking, suggesting depression-related impairments in the processing of emotional stimuli. [ABSTRACT FROM AUTHOR]

Elevated markers of peripheral inflammation are common in psychosis spectrum disorders and have been associated with brain anatomy, pathology, and physiology as well as clinical outcomes. Preliminary evidence suggests a link between inflammatory cytokines and C-reactive protein (CRP) with generalized cognitive impairments in a subgroup of individuals with psychosis. Whether these patients with elevated peripheral inflammation demonstrate deficits in specific cognitive domains remains unclear. To examine this, seventeen neuropsychological and sensorimotor tasks and thirteen peripheral inflammatory and microvascular markers were quantified in a subset of B-SNIP consortium participants (129 psychosis, 55 healthy controls). Principal component analysis was conducted across the inflammatory markers, resulting in five inflammation factors. Three discrete latent cognitive domains (Visual Sensorimotor, General Cognitive Ability, and Inhibitory Behavioral Control) were characterized based on the neurobehavioral battery and examined in association with inflammation factors. Hierarchical clustering analysis identified cognition-sensitive high/low inflammation subgroups. Among persons with psychotic disorders but not healthy controls, higher inflammation scores had significant associations with impairments of Inhibitory Control (R2 = 0.100, p -value = 2.69e−4, q -value = 0.004) and suggestive associations with Visual Sensorimotor function (R2 = 0.039, p -value = 0.024, q -value = 0.180), but not with General Cognitive Ability (R2 = 0.015, p -value = 0.162). Greater deficits in Inhibitory Control were observed in the high inflammation patient subgroup, which represented 30.2 % of persons with psychotic disorders, as compared to the low inflammation psychosis subgroup. These findings indicate that inflammation dysregulation may differentially impact specific neurobehavioral domains across psychotic disorders, particularly performance on tasks requiring ongoing behavioral monitoring and control. [ABSTRACT FROM AUTHOR]

• ELA moderates the association between frequency and inhibitory control. • Association is positive for high and low Uyghur and Mandarin ELA children. • Association is negative for low Uyghur and Mandarin ELA children. Although research has indicated the contribution of bilinguals' language switching frequency and language abilities to their inhibitory control, the mechanism of how they work together to influence inhibitory control is unclear. This study examined the moderating role of expressive and receptive language abilities on the relationship between language switching frequency and inhibitory control. Participants were 229 Uyghur-Mandarin bilingual preschoolers aged 4.5 to 6.5 years. They were individually tested on expressive language ability (ELA), receptive language ability (RLA), and inhibitory control. Their frequency of language switching was collected from parents' and teachers' reports. The results showed that language switching frequency was positively associated with inhibitory control in children with high Uyghur ELA and low Mandarin ELA, and vice versa. Moreover, language switching frequency was negatively associated with inhibitory control in children with both low Uyghur and Mandarin ELA, but not significantly associated with inhibitory control in children with both high Uyghur and Mandarin ELA. Additionally, this moderating effect of language abilities was not found in receptive language abilities. The significant moderating effect of ELA, but not RLA, suggests the active role of children in their early executive function development; this extends the current understanding of how and when language switching frequency impacts bilinguals' inhibitory control. [ABSTRACT FROM AUTHOR]

Adaptive behavior depends on the delicate and dynamic balance between acquisition and extinction memories. Disruption of this balance, particularly when the extinction of memory loses control over behavior, is the root of treatment failure of maladaptive behaviors such as substance abuse or anxiety disorders. Understanding this balance requires a better understanding of the underlying neurobiology and its contribution to behavioral regulation. We microinjected Daun02 in Fos-lacZ transgenic rats following a single extinction training episode to delete extinction-recruited neuronal ensembles in the basolateral amygdala (BLA) and central nucleus of the amygdala (CN) and examined their contribution to behavior in an appetitive Pavlovian task. In addition, we used immunohistochemistry and neuronal staining methods to identify the molecular markers of activated neurons in the BLA and CN during extinction learning or retrieval. CN neurons were preferentially engaged following extinction, and deletion of these extinction-activated ensembles in the CN but not the BLA impaired the retrieval of extinction despite additional extinction training and promoted greater levels of behavioral restoration in spontaneous recovery and reinstatement. Disrupting extinction processing in the CN in turn increased activity in the BLA. Our results also show a specific role for CN PKCδ+ neurons in behavioral inhibition but not during initial extinction learning. We showed that the initial extinction-recruited CN ensemble is critical to the acquisition-extinction balance and that greater behavioral restoration does not mean weaker extinction contribution. These findings provide a novel avenue for thinking about the neural mechanisms of extinction and for developing treatments for cue-triggered appetitive behaviors. [ABSTRACT FROM AUTHOR]

Individuals with bipolar I disorder (BD) have difficulty inhibiting context-inappropriate responses. However, neural mechanisms of impaired cognitive control over impulsive behaviors, especially in response to emotion, are unclear. Theta-band neural oscillatory activity over midfrontal areas is thought to reflect cognitive control. The current study examined behavioral performance and theta-band activity during inhibition to affective stimuli in BD, relative to healthy control participants (HC). Sixty-seven participants with BD and 48 HC completed a Go/No-Go task with emotional face stimuli during electroencephalography (EEG) recording. Behavior was measured with reaction time, discriminability (d') and response bias (β). Time-frequency decomposition of EEG data was used to extract event-related theta-band (4–7 Hz) neural oscillatory power and inter-trial phase consistency (ITPC) over midline fronto-central areas. Behavior and theta-band activity were compared between groups, while covarying for age. Participants with BD exhibited slower response execution times on correct Go trials and reduced behavioral discrimination of emotional versus neutral faces, compared to HC. Theta-band power and ITPC were reduced in BD relative to HC. Theta-band power was higher on No-Go trials than Go trials. The magnitude of differences in theta-band activity between Go/No-Go trial types did not differ between groups. Increased theta-band power was associated with faster response execution times, greater discrimination of differing facial expressions, and stronger tendency to respond both across the full sample and within the BD group. Attenuated midline fronto-central theta-band activity may contribute to reduced cognitive control and maladaptive behavioral responding to emotional cues in individuals with BD. [ABSTRACT FROM AUTHOR]

• Categorizing and managing unusual responses to PCSK9 inhibition. The efficacy of proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibition has broadened lipid-lowering therapy thus providing decreased risk in atherosclerotic cardiovascular disease. Unfortunately, the widespread use of PCSK9 inhibitors (PCSK9i), ie, monoclonal antibodies, has led to the findings of unusual responsiveness, ie, a phenomenon defined as an LDL-C reduction of <30% vs the average LDL-C reduction efficacy of 50–60%. This unusual responsiveness to PCSK9i is attributable to several factors, ie, lack of adherence, impaired absorption, poor distribution or early elimination as well as abnormal effects of PCSK9i in the presence of anti-antibodies or mutations in PCSK9 and LDLR. Unexpectedly increased lipoprotein (Lp)(a) also appear to contribute to the unusual responsiveness scenario. Identification of these responses and mechanisms underlying them are essential for effective management of LDL-C and cardiovascular risk. In this review, we describe plausible reasons underlying this phenomenon supported by findings of clinical trials. We also elaborate on the need for education and regular follow-up to improve adherence. Collectively, the review provides a summary of the past, present, and future of mechanisms and countermeasures revolving around unusual responses to PCSK9i therapy. [ABSTRACT FROM AUTHOR]

Cross-sectional group comparisons have shown altered neurocognitive and neurophysiological profiles in individuals with attention-deficit/hyperactivity disorder (ADHD). We report a two-year longitudinal observational study of ADHD children and adolescents (N = 239) regarding ADHD symptoms, behavioral metrics, and event-related potentials (ERP) and compared them to healthy controls (N = 91). The participants were assessed up to five times with a cued Go/NoGo task while ERPs were recorded. We fitted the trajectories of our variables of interest with univariate and bivariate latent growth curve models. At baseline, the ADHD group had increased reaction time variability, higher number of omission and commission errors, and attenuated CNV and P3d amplitudes compared to controls. The task performance in terms of behavioral metrics improved in both groups over two years; however, with differential patterns: the decrease in reaction time and omission errors were stronger in the control group, and the reduction of commission errors was more substantial in the ADHD group. The cueP3, CNV, and N2d amplitudes changed slightly over two years, with negligible differences between both groups. Furthermore, the parent-rated symptom burden in the ADHD group decreased by 22 % (DSM-5-based questionnaire). We did not identify any associations between the changes in symptoms and the changes in the behavioral or neurophysiological metrics. The lack of association between the changes in symptoms and the behavioral or ERP metrics supports the trait liability hypothesis, which claims that the neurocognitive deficits are independent of symptom alleviation. Furthermore, the change in symptom burden was substantial, questioning the stability of the reported ADHD symptoms. • Individuals with ADHD perform worse in tests of attention and inhibitory control. • Altered neurophysiology (ERPs) in individuals with vs. without ADHD • Comparable development in individuals with & without ADHD over two years • Strong symptom reduction (22 %) in the ADHD group over two years [ABSTRACT FROM AUTHOR]

Excessive fear responses to uncertain threat are a key feature of anxiety disorders (ADs), though most mechanistic work considers adults. As ADs onset in childhood and confer risk for later psychopathology, we sought to identify conditions of uncertain threat that distinguish 8–17-year-old youth with AD (n = 19) from those without AD (n = 33), and assess test-retest reliability of such responses in a companion sample of healthy adults across three sites (n = 19). In an adapted uncertainty of threat paradigm, visual cues parametrically signaled threat of aversive stimuli (fear faces) in 25 % increments (0 %, 25 %, 50 %, 100 %), while participants underwent functional magnetic resonance imaging (fMRI). We compared neural response elicited by cues signaling different degrees of probability regarding the subsequent delivery of fear faces. Overall, youth displayed greater engagement of bilateral inferior parietal cortex, fusiform gyrus, and lingual gyrus during uncertain threat anticipation in general. Relative to healthy youth, AD youth exhibited greater activation in ventrolateral prefrontal cortex (vlPFC)/BA47 during uncertain threat anticipation in general. Further, AD differed from healthy youth in scaling of ventral striatum/sgACC activation with threat probability and attenuated flexibility of responding during parametric uncertain threat. Complementing these results, significant, albeit modest, cross-site test-retest reliability in these regions was observed in an independent sample of healthy adults. While preliminary due to a small sample size, these findings suggest that during uncertainty of threat, AD youth engage vlPFC regions known to be involved in fear regulation, response inhibition, and cognitive control. Findings highlight the potential of isolating neural correlates of threat anticipation to guide treatment development and translational work in youth. • In an adapted uncertainty of threat fMRI paradigm, visual cues parametrically signaled threat of aversive stimuli. • We noted greater engagement of vlPFC during uncertain threat anticipation in youth with anxiety disorders vs healthy youth. • We also observed reduced ventral striatum activation during threat probability in anxious vs healthy youth. • We relate group level findings to test-retest reliability in adults. [ABSTRACT FROM AUTHOR]

Attention deficit hyperactivity disorder (ADHD) is involved in broad neuropsychological domains, including response inhibition, timing, delay aversion, sustained attention, and working memory. This study aimed to examine the relationship between ADHD symptoms and neuropsychological measures in university students. A total of 167 graduate and undergraduate students participated in the study. Neuropsychological characteristics were comprehensively assessed using stop signal, delay discounting, time discrimination, sensorimotor synchronization, continuous performance, and digit span tasks. ADHD symptoms were assessed using the Japanese version of Conners' ADHD Rating Scale. ADHD symptoms were significantly correlated with some neuropsychological measures, such as the false alarm rate in the continuous performance task; however, these correlations were not strong. In the multiple regression analyses, models including neuropsychological measures were significantly associated with ADHD symptoms, but the coefficients of determination ranged from 0.06 to 0.08. Thus, most of the variance in ADHD symptoms was not explained by neuropsychological measures. These findings suggest that the impact of each neuropsychological measure on ADHD symptoms was weak in university students, and ADHD symptoms cannot be explained by neuropsychological characteristics, which are currently considered core characteristics of ADHD. In addition, ADHD symptoms assessed by self-rating questionnaire in the non-clinical sample might not reflect the degree of real ADHD severity. [ABSTRACT FROM AUTHOR]

Objective: Behavioral inhibition (BI) is an infant temperament characterized by heightened reactivity and negative affect in response to novel people and situations. BI is among the earliest and strongest predictors of future anxiety problems. However, not all children with a history of BI will manifest anxiety problems. A growing body of evidence suggests that proactive control skills may help buffer youth with BI from future anxiety difficulties; yet, it remains unclear how temperament may interact with the development of cognitive control to influence anxiety risk. The present study tested whether enhancements in proactive control occurring during adolescence may reduce risk for anxiety among youth with a history of BI.Method: Participants included 185 adolescents (56% female) whose temperament was assessed during toddlerhood. In adolescence, participants completed anxiety assessments and an AX Continuous Performance Test (AX-CPT) to assess cognitive control strategy. Both assessments were administered at age 13 years and again at 15 years.Results: Latent change score modeling revealed that, on average, participants increasingly used proactive control strategies and experienced worsening anxiety from age 13-15 years. Early BI was associated with a smaller anxiety increase from 13-15 years, but only among participants whose proactive control skills improved at mean or greater rates.Conclusion: The present findings suggest that greater proactive control development during adolescence protects youth with high BI from age-related increases in anxiety. Results support a framework that highlights cognitive control as a key moderator of anxiety risk among children with a history of high BI. [ABSTRACT FROM AUTHOR]

Background Most previous work has focused on a single-nutrient, bottom-up approach when examining the influence of diet on neurocognition. Thus, the impact of dietary patterns on cognitive health is underinvestigated. Objectives We aimed to investigate the relation between different diet indices [i.e., Mediterranean, Dietary Approaches to Stop Hypertension (DASH), Healthy Eating Index-2015 (HEI-2015), and Mediterranean-DASH Intervention for Neurodegenerative Delay (MIND)] and attentional inhibition and neuroelectric function. Methods We undertook a cross-sectional analysis of adults aged 34.1 ± 6.0 y (n  = 207, 116 females) with a BMI of 18.5 to >40 kg/m2 who completed the Dietary History Questionnaire II (DHQII) FFQ (Past Month and Year with Serving Sizes) to assess adherence to different diet quality indices. Attentional inhibition was assessed using a modified Eriksen flanker task during which event-related potentials (ERPs) were recorded. The amplitude and latency of the P3/P300 ERP were used to index attentional resource allocation and information processing speed, respectively. Results P3 peak latency was inversely associated with greater adherence to the MIND dietary pattern during incongruent flanker trials (∆R2  = 0.02, β = −0.14, P  = 0.043) but not during congruent trials. Adherence to the Mediterranean, DASH, and HEI-2015 patterns was not associated with P3 latency (P  > 0.05). No associations were observed between the diet indices and attentional inhibition at the behavioral level (i.e., accuracy or reaction time) or P3 amplitude (all P  values >0.05). Conclusions Greater adherence to the MIND diet was selectively associated with faster information processing speed in middle-aged adults with healthy to obese BMI. Further, the influence of the MIND diet for faster information processing speed might be particularly beneficial when cognitive control demands are increased. Future intervention trials testing the effects of consuming a MIND diet on cognitive function are warranted to help inform dietary recommendations for healthy cognitive aging. [ABSTRACT FROM AUTHOR]

• We studied effects of deep brain stimulation in subthalamic nucleus and globus pallidus on action control processes. • Stimulation in both targets induces fast impulsive action errors. • Stimulation in the subthalamic nucleus and globus pallidus also improves selective inhibitory control. Deep brain stimulation (DBS) is an effective treatment to improve motor symptoms in Parkinson's disease (PD). The Globus Pallidus (GPi) and the Subthalamic Nucleus (STN) are the most targeted brain regions for stimulation and produce similar improvements in PD motor symptoms. However, our understanding of stimulation effects across targets on inhibitory action control processes is limited. We compared the effects of STN (n = 20) and GPi (n = 13) DBS on inhibitory control in PD patients. We recruited PD patients undergoing DBS at the Vanderbilt Movement Disorders Clinic and measured their performance on an inhibitory action control task (Simon task) before surgery (optimally treated medication state) and after surgery in their optimally treated state (medication plus their DBS device turned on). DBS to both STN and GPi targets induced an increase in fast impulsive errors while simultaneously producing more proficient reactive suppression of interference from action impulses. Stimulation in GPi produced similar effects as STN DBS, indicating that stimulation to either target increases the initial susceptibility to act on strong action impulses while concomitantly improving the ability to suppress ongoing interference from activated impulses. Action impulse control processes are similarly impacted by stimulating dissociable nodes in frontal-basal ganglia circuitry. [ABSTRACT FROM AUTHOR]

Although the primary aetiology of Eating Disorders (ED) remains unknown, research suggests a complex interplay of biological, psychological, and cultural/environmental factors. This paper aims to systematically review the literature on neuroimaging studies that measure socio-cognitive factors, in the context of body dissatisfaction and EDs in young people. Specifically, our aim was to identify patterns in the findings linked to social media-type behaviours. The review was conducted in accordance with PRISMA guidelines using PubMed, Scopus, and Web of Science databases. 799 papers were identified in the database search and 38 studies were selected based on exclusion and inclusion criteria. Selected studies were assessed using the National Institute of Health study quality assessment tool. Findings point to state-related impairments in inhibitory control and salient emotional processing. Anorexia Nervosa(AN) showed impaired set-shifting abilities, working memory and decision making, while altered activation in attention networks and associated difficulties with conflict resolution were seen for Bulimia Nervosa(BN) and Other Specified Feeding and Eating Disorders(OSFED). AN and BN also demonstrated altered sensitivity to food-related stimuli in striatal regions, suggesting aberrant top-down emotional-cognitive control. ED participants also show deficits in body representation, impaired control over social behaviours and altered integration of visual and body perception. These findings support the notion that socio-cognitive dysfunctions in ED are underpinned by a distributed network of structural and functional brain changes which influence the way young people with ED interact with and respond to social media, and ultimately places at them at increased risk for body image disturbances. This Review was registered with the PROSPERO International Register of Systematic Reviews, Registration number CRD42021270696. [ABSTRACT FROM AUTHOR]

The NoGo P3 event-related potential (ERP) component is often related to response inhibition, although its function in equiprobable Go/NoGo tasks is debated. Previous findings concerning the auditory equiprobable NoGo P3 (or P3a) could be distorted by averaging latency-variable ERP components. This study aimed to control NoGo P3 latency jitter to investigate the component's relationship with inhibitory demands and its neuronal sources across trials. P3 latency jitter was controlled using a novel procedure to enable single-trial P3 quantification across 126 healthy young adults (M age = 20.3, SD = 2.8 years) using principal components analysis. NoGo inhibitory demands and performance were measured using the Lateralised Readiness Potential and error rates, respectively. The stimulus-locked P3 (SL-P3) was also analysed to assess the 'blurring effect' (i.e., smearing) associated with averaging latency-variable ERP trial data. A Spearman's rank correlation across 4700 NoGo trials demonstrated that the relationship between latency-adjusted P3 (LA-P3) and inhibitory demands was inconsequential. The cortical sources associated with LA-P3, using eLORETA, were in the premotor and prefrontal cortices, cingulate, and precuneus. SL-P3 was smaller than LA-P3, and that difference was positively related to P3 latency jitter; its source solution was also limited to lower activation in the prefrontal cortex. SL-P3 was not related to inhibitory demands or performance. This study indicates that NoGo P3 should not index response inhibition in auditory equiprobable tasks. Instead, the findings support a neuroinhibition account relating NoGo P3 to attention. Blurring effects were also shown to impact a standard ERP measure and its source solution, encouraging ERP latency-adjustment in future research. • The auditory equiprobable NoGo P3 should not index motor inhibition in healthy adults. • NoGo P3 could reflect an attention shift related to performance monitoring. • ERP latency jitter significantly impacted P3 amplitudes and cortical source analyses. • ERP blurring effects are minimised using single-trial latency adjusted ERP analyses. • Equiprobable Go/NoGo tasks are unsuitable for studying inhibition in healthy adults. [ABSTRACT FROM AUTHOR]