ArticleLiterature Review

Frozen in (e)motion: How reactive motor inhibition is influenced by the emotional content of stimuli in healthy and psychiatric populations

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Abstract

Efficient inhibitory control is vital. However, environmental cues can influence motor control especially in an emotional context. One common task to measure inhibitory control is the stop-signal task (SST), which asks participants to respond to go stimuli knowing that on some trials a stop signal will be presented, requiring them to inhibit their response. This paradigm estimates the ability to inhibit already-initiated responses by calculating participants' stop-signal reaction times (SSRT), an index of inhibitory control. Here, we aim to review the existing, often contradictory, evidence on the influence of emotional stimuli on the inhibitory process. We aim to discuss which factors may reveal an interference as well as an advantage of emotional stimuli on action inhibition performance. Finally, we review the existing evidence that has investigated the effect of such stimuli on action inhibition in the psychiatric population. Important factors are the relevance, the intensity and the valence of the emotional stimulus, as well as the affected component of the motor control. From all this evidence, it is clear that understand precisely how emotion is integrated into core executive functions, such as inhibitory control, is essential not only for cognitive neuroscience, but also for refining neurocognitive models of psychopathology.

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... A body of recent research has argued that the mere perception of a threat may cause a temporary halt in any ongoing movement (i.e. freezing) that in some cases causes a slower reaction time-that is, delayed avoidance, presumably because the threat automatically draws attentional and cognitive resources (Battaglia et al., 2021;Borgomaneri et al., 2015;Cao & Liu, 2021;de Houwer & Tibboel, 2010;Liu et al., 2017;Mancini et al., 2020;Mirabella, 2018). ...
... We found longer movement preparation times in snake-fearful participants when the movement was initiated from the snake picture. This is in line with previous studies showing that threats perceived as more imminent capture attention involuntarily (Arnaudova et al., 2017), and this could result in a temporary motor freezing (Battaglia et al., 2021;Borgomaneri et al., 2015). The freezing response-if active-can help potential prey when assessing the threat and preparing for subsequent movements (Gladwin et al., 2016;Rösler & Gamer, 2019). ...
... showing that the defensive temporary freezing primarily occurs when the threat appears outside of foveal vision (Arnaudova et al., 2017;Battaglia et al., 2021;Borgomaneri et al., 2015;Gladwin et al., 2016). ...
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How people experience nature influences their attitudes and actions towards it. Having had a negative encounter with an animal may facilitate avoidance and freezing responses which may encourage negative feelings towards it and the environment in which it is found. Animals associated with fear, such as snakes, are often the victims of hunting and killing, possibly in part due to an overperception of their inherent danger. Past research has shown that fear affects approach–avoidance response at both the preparatory and executive stages of movement. However, the way one reacts to different threats may also depend on its proximity and how fearful one is of that specific threat. We employed a mouse‐tracking paradigm where participants (N = 40) categorized pictures of threatening and non‐threatening animals (snakes and butterflies respectively). The picture could appear at the middle, top or bottom of the screen. Participants initiated the movement from the centre of the screen and the category labels appeared on the top of the screen. Participants therefore had to either move towards the picture on the top or move away from the picture (presented centrally or at the bottom). Participants were split into fearful and non‐fearful groups based on self‐report snake fear. Non‐fearful participants were generally slower when a threat was present. But, in the fearful group, we found longer movement initiation times for central threats and shorter initiation times for off‐centre threats (compared to neutral targets). Fearful participants were also slower to initiate movement when moving away from the threat, but faster when moving towards it (compared to neutral targets). The slower start and execution may be due to the lack of active planning and/or may imply the presence of a passive temporary freezing response. Strong negative emotions towards nature and animals serve as crucial factors both in animal phobias and anti‐animal behaviours (i.e. the purposeful decimation of certain species). Understanding the action dynamics of approach–avoid behaviours in response to threatening animals may help to inform both the prevention and treatment of phobias, and relatedly, the promotion of conservationist endeavours. Read the free Plain Language Summary for this article on the Journal blog.
... Furthermore, different personality states of the participants were investigated, as previous studies have shown that SST performance, as well as reactive action inhibition, may be influenced by psychological or psychiatric conditions (i.e., anxiety, depression, impulsivity) (Pessoa et al., 2012;Legrand and Price, 2020;Battaglia et al., 2021). Subjective levels of anxiety were measured through the State-Trait Anxiety Inventory (STAI; Trait-Scale-Y2) (Spielberger et al., 1983) and subjective levels of impulsivity were measured by the Barratt Impulsiveness Scale-11 (BIS-11) (Patton et al., 1995). ...
... The processing of emotion-laden information, such as threat, is fast and prioritized. Indeed, negative stimuli have been found to rapidly suppress cortical or corticospinal excitability (Borgomaneri et al., 2015b(Borgomaneri et al., ,c, 2017(Borgomaneri et al., , 2020bVicario et al., 2017;Battaglia et al., 2021), which has been interpreted as a freezing-like inhibitory modulation of the primary motor cortex (Borgomaneri et al., 2015a). In line with this negative advantage effect, several studies have tried to disclose the impact of fearful stimuli over one of the fundamental executive human capabilities, namely the ability to inhibit an inappropriate action (Bari and Robbins, 2013;Mirabella, 2014). ...
... Several areas in the prefrontal cortex have been associated with the mechanisms underlying inhibitory control, with a network including the inferior frontal gyrus (IFG), primary motor area (Mattia et al., 2012), pre-motor area (Cattaneo and Parmigiani, 2021), pre-supplementary motor area (pre-SMA; see Wessel and Aron, 2017;Zhang et al., 2017;Borgomaneri et al., 2020a for a comprehensive meta-analysis), posterior parietal cortex (Convento et al., 2014), and basal ganglia (Mallet et al., 2016). Indeed, several studies have attempted to disclose the crucial nodes involved in action control (Wessel et al., 2013;Mirabella et al., 2020) or in the control of fear responses (Borgomaneri et al., 2020b) by employing non-invasive brain stimulation techniques (NIBS) (Borgomaneri et al., 2020b;Battaglia et al., 2021). Recently, there has been a growing interest in the use of NIBS to selectively manipulate the activations of selective brain regions of the action inhibition network (AIN) to investigate their specific contribution to many processes underlying action control (i.e., inhibition, selection, competition, and switching of actions). ...
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Since the dawn of cognitive neuroscience, emotions have been recognized to impact on several executive processes, such as action inhibition. However, the complex interplay between emotional stimuli and action control is not yet fully understood. One way to measure inhibitory control is the stop-signal task (SST), which estimates the ability to cancel outright an action to the presentation of a stop signal by means of the stop-signal reaction times (SSRTs). Impaired as well as facilitated action control has been found when faced with intrinsic emotional stimuli as stop signals in SSTs. Here, we aimed at investigating more deeply the power of negative stimuli to influence our action control, testing the hypothesis that a previously neutral stimulus [i.e., the image of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)], which has been conditioned through vicarious fear learning, has the same impact on reactive action inhibition performance as an intrinsically negative stimulus (i.e., a fearful face or body). Action control capabilities were tested in 90 participants by means of a SST, in which the stop signals were represented by different negative stimuli. Results showed that the SARS-CoV-2 image enhanced the ability to suppress an ongoing action similarly to observing fearful facial expressions or fearful body postures. Interestingly, we found that this effect was predicted by impulsivity traits: for example, the less self-control the participants had, the less they showed emotional facilitation for inhibitory performance. These results demonstrated that vicarious fear learning has a critical impact on cognitive abilities, making a neutral image as threatening as phylogenetically innate negative stimuli and able to impact on our behavioral control.
... Several studies using SST have aimed to uncover the influence of emotional stimuli on action control capabilities. However, findings are inconsistent, as these investigations collectively reveal that emotion can either impair, facilitate, or have no effect on action control (for a review see Battaglia et al., 2021). A factor that might have influenced the divergent outcomes is the varied functions of the emotional stimulus, such as being presented as a stop signal, go signal, or as a prime before the go signal. ...
... The ANOVA results confirmed the main effect of the Prime factor [F(1, 42) = 4.78, p = 0.03 ηp 2 = 0.79], while the main effect of the factor Group was not found to be significant [F(1, 42) = 0.07, p = 0.79, ηp 2 = 0.01], nor was the Prime × Group interaction [F(1, 42) = 1.13, p = 0.29, ηp 2 = 0.18]. These results are in line with previous findings, which demonstrate that action control is influenced by the presence of emotional stimuli (see Battaglia et al., 2021 for a review on the topic) but, crucially, our findings demonstrated that such effects are detectable even when the negative arousing stimuli are not consciously perceived, corroborating to the idea that consciousness of the emotional stimuli is not a prerequisite to observe an influence on behavior. To assess whether differences in participants' impulsivity may have an impact on the results, we conducted an analysis using a Generalized Linear Mixed Model with Prime, BIS-11, and their interaction as fixed effects and subject as a random effect. ...
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Efficient inhibitory control in the context of prepotent actions is vital. However, such action inhibition may be profoundly influenced by affective states. Interestingly, research indicates that action control can be either impaired or improved by emotional stimuli. Thus, a great deal of confusion surrounds our knowledge of the complex dynamics subtending emotions and action control. Here, we aimed to investigate whether negative stimuli, even when non-consciously presented and task-irrelevant, can affect action control relative to neutral stimuli. Additionally, we tested whether individual differences in intracortical excitability may predict action control capabilities. To address these issues, we asked participants to complete a modified version of the Stop Signal Task (SST) in which fearful or neutral stimuli were subliminally presented before the go signals as primes. Moreover, we assessed participants’ resting-state corticospinal excitability, short intracortical inhibition (SICI), and intracortical facilitation (ICF). Results demonstrated better action control capabilities when fearful stimuli were subliminally presented and interindividual SICI predicted stronger action inhibition capabilities. Taken together, these results shed new light on the intricate dynamics between action, consciousness, and motor control, suggesting that intracortical measures can be used as potential biomarkers of reduced motor inhibition in research and clinical settings.
... [48][49][50][51][52][53][54][55][56] Indeed, several SST studies have demonstrated that emotions can influence action inhibition. However, they reported both the enhancement and impairment of action control (i.e., increase or decrease in SSRT) by emotions (for a review, see Ref. 57). Additionally, some evidence shows no influence of emotional stimuli in inhibitory performance. ...
... In addition, different personality traits of the participants were investigated as previous studies have shown that SST performance, as well as reactive action inhibition, may be influenced by psychological or psychiatric conditions (i.e., anxiety, depression, impulsivity, addiction). 57 Figure S1; see Table 2 for further details). Importantly, data collection was anonymous, and all participants gave their informed consent electronically through our online platform before the task. ...
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Swiftly halting ongoing motor actions is essential to react to unforeseen and potentially perilous circumstances. However, the neural bases subtending the complex interplay between emotions and motor control have been scarcely investigated. Here, we used an emotional stop signal task (SST) to investigate whether specific neural circuits engaged by action suppression are differently modulated by emotional signals with respect to neutral ones. Participants performed an SST before and after the administration of one session of repetitive transcranial magnetic stimulation (rTMS) over the pre‐supplementary motor cortex (pre‐SMA), the right inferior frontal gyrus (rIFG), and the left primary motor cortex (lM1). Results show that rTMS over the pre‐SMA improved the ability to inhibit prepotent action (i.e., better action control) when emotional stimuli were presented. In contrast, action control in a neutral context was fostered by rTMS over the rIFG. No changes were observed after lM1 stimulation. Intriguingly, individuals with higher impulsivity traits exhibited enhanced motor control when facing neutral stimuli following rIFG stimulation. These results further our understanding of the interplay between emotions and motor functions, shedding light on the selective modulation of neural pathways underpinning these processes.
... The most commonly affected cognitive domains are cognitive processing speed and episodic memory [8]. An interesting facet that should be considered is that different psychopathological conditions are characterized by severe impulsivity problems that can contribute to causing disability due to poor regulation and control, which can become worse in the presence of emotional cues [9]. Interestingly, emotions could ameliorate or disturb motor inhibition ability [9]. ...
... An interesting facet that should be considered is that different psychopathological conditions are characterized by severe impulsivity problems that can contribute to causing disability due to poor regulation and control, which can become worse in the presence of emotional cues [9]. Interestingly, emotions could ameliorate or disturb motor inhibition ability [9]. Of note, a great deal of evidence, additionally supported by studies of brain-damaged patients, has suggested that the superior temporal sulcus could have a role in attentional orienting, whereas the amygdala could be involved in jointly elaborating gaze and emotional expressions [10]. ...
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Multiple sclerosis (MS) is an autoimmune neurodegenerative disorder of the central nervous system that presents heterogeneous clinical manifestations and course. It has been shown that different immune checkpoints, including Cytotoxic T-Lymphocyte Antigen 4 (CTLA-4), can be involved in the pathogenesis of MS. CTLA-4 is a critical regulator of T-cell homeostasis and self-tolerance and represents a key inhibitor of autoimmunity. In this scopingreview, we resume the current preclinical and clinical studies investigating the role of CTLA-4 in MS with different approaches. While some of these studies assessed the expression levels of CTLA-4 on T cells by comparing MS patients with healthy controls, others focused on the evaluation of the effects of common MS therapies on CTLA-4 modulation or on the study of the CTLA-4 blockade or deficiency in experimental autoimmune encephalomyelitis models. Moreover, other studies in this field aimed to discover if the CTLA-4 gene might be involved in the predisposition to MS, whereas others evaluated the effects of treatment with CTLA4-Ig in MS. Although these results are of great interest, they are often conflicting. Therefore, further studies are needed to reveal the exact mechanisms underlying the action of a crucial immune checkpoint such as CTLA-4 in MS to identify novel immunotherapeutic strategies for MS patients.
... Successful motor inhibition to threat signals increased activation in limbic regions (amygdala), SMA, in a region in the lateral orbitofrontal cortex, distinct from areas in the IFG typically associated with voluntary inhibition. The ability to voluntarily inhibit unnecessary actions is an important aspect in psychiatric disorders [27]. Deficits in performance in action control have been observed in various psychiatric disorders, which are characterized by serious impulsivity problems that can determine significant impairment or distress. ...
... Deficits in performance in action control have been observed in various psychiatric disorders, which are characterized by serious impulsivity problems that can determine significant impairment or distress. These psychopathological conditions included schizophrenia, bipolar disorder, and ADHD [26,27]. Some patients with FLE display a pattern of behavioral and cognitive impairment that may be linked to an epilepsy-related deterioration of these networks [28]. ...
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Background Attention Deficit Hyperactivity Disorder (ADHD) is a prevalent neurological disorder. ADHD has been linked to epilepsy. Main body ADHD was found to be present in 30–40% of epileptic children. Researchers have developed numerous theories to explain how and why ADHD and epilepsy coexist. Whether ADHD and epilepsy symptoms are caused by co-occurring psychiatric disorders or by the temporary effects of epileptic discharges or by antiepileptic medicines is critical to consider. Diagnosis and treatment of individuals with ADHD and epilepsy are complicated and challenging from the clinical base. Conclusions Comorbidity between ADHD and epilepsy is still challenging to understand. The two diseases have a bidirectional link, so the association may not be coincidental. A disputable point is whether co-occurring ADHD and epilepsy symptoms represent a comorbid psychiatric disorder or are the epileptic discharges’ temporary effects, and are they related to antiepileptic drugs (AEDs). It is recommended to follow up with children with epilepsy or ADHD as they may develop comorbidity after a while.
... Although different studies have investigated multiple factors involved in value computation [47,52,[73][74][75][76], including risk [77,78], spatial distance [79][80][81], effort [9-12,82] and temporal discounting [15][16][17][18], little is known about how the cost of an action impacts on valuation processes. This study describes a new experimental protocol for studying and quantifying how such cost can affect valuation processes and, thus, behaviour. ...
... Although different studies have investigated multiple factors involved in value computation [47,52,[73][74][75][76], including risk [77,78], spatial distance [79][80][81], effort [9][10][11][12]82] and temporal discounting [15][16][17][18], little is known about how the cost of an action impacts on valuation processes. This study describes a new experimental protocol for studying and quantifying how such cost can affect valuation processes and, thus, behaviour. ...
Article
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Growing evidence suggests that humans and other animals assign value to a stimulus based on its inherent rewarding properties, but also on the costs of the action required to obtain it, such as the cost of time. Here, we examined whether such cost also occurs for mentally simulated actions. Healthy volunteers indicated their subjective value for snack foods while the time to imagine performing the action to obtain the different stimuli was manipulated. In each trial, the picture of one food item and a home position connected through a path were displayed on a computer screen. The path could be either large or thin. Participants first rated the stimulus, and then imagined moving the mouse cursor along the path, from the starting position to the food location. They reported the onset and offset of the imagined movements with a button press. Two main results emerged. First, imagery times were significantly longer for the thin than the large path. Second, participants liked significantly less the snack foods associated with the thin path (i.e., with longer imagery time), possibly because the passage of time strictly associated with action imagery discounts the value of the reward. Importantly, such effects were absent in a control group of participants who performed an identical valuation task, except that no action imagery was required. Our findings hint at the idea that imagined actions, like real actions, carry a cost that affects deeply how people assign value to the stimuli in their environment.
... In fact, while the classic cognitive profile of AD is mainly characterised by episodic memory deficits due to the impairment of the temporal lobe, several recent studies have shown that in relation to the different brain areas predominantly involved, different clinical pictures may be present. For example, alterations in the medial prefrontal cortex are associated with impaired retrieval and extinction memories, whereas impairment of emotional and executive processing, similarly to the psychiatric population, reflects a probable impairment of the lateral orbitofrontal cortex or the inferior frontal gyrus [6][7][8]. It is worth underlining that multiple pathways are implicated in the onset and progression of neurodegeneration and specific functions, such as emotional control, are often impaired in dementia. ...
... It is worth underlining that multiple pathways are implicated in the onset and progression of neurodegeneration and specific functions, such as emotional control, are often impaired in dementia. Indeed, impairment of the prefrontal cortex causes in AD patients an impairment in emotion processing that impacts on action and motor control [7]. ...
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Alzheimer’s disease (AD) is the most common type of dementia, affecting 24 million individuals. Clinical and epidemiological studies have found several links between vascular risk factors (VRF), neurovascular unit dysfunction (NVUd), blood-brain barrier breakdown (BBBb) and AD onset and progression in adulthood, suggesting a pathogenetic continuum between AD and vascular dementia. Shared pathways between AD, VRF, and NVUd/BBB have also been found at the molecular level, underlining the strength of this association. The present paper reviewed the literature describing commonly shared molecular pathways between adult-onset AD, VRF, and NVUd/BBBb. Current evidence suggests that VRF and NVUd/BBBb are involved in AD neurovascular and neurodegenerative pathology and share several molecular pathways. This is strongly supportive of the hypothesis that the presence of VRF can at least facilitate AD onset and progression through several mechanisms, including NVUd/BBBb. Moreover, vascular disease and several comorbidities may have a cumulative effect on VRF and worsen the clinical manifestations of AD. Early detection and correction of VRF and vascular disease by improving NVUd/BBBd could be a potential target to reduce the overall incidence and delay cognitive impairment in AD.
... This impairment in cognitive functions is due to anatomical atrophy of AD brains, which correlates with severe neuronal loss [5]. In particular, the lack of good coordination within structures like prefrontal cortex, hippocampus and amygdala seems to play a predominant role in cognitive deficits in the advanced age [6]. ...
... It is now recognized that TDP-43 deposition increases the risk for developing AD and influences the clinical features of dementia including cognitive deficits [26]. In addition, the fact that TDP-43 deposits are more abundant in the limbic system suggest a possible role of TDP-43 in the action control and emotion processing impaired in AD due to atrophy of prefrontal cortex and limbic system [6]. ...
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Alzheimer’s disease (AD) is a neurodegenerative disorder for which there is currently no effective treatment. Despite advances in the molecular pathology of the characteristic histopathological markers of the disease (tau protein and β-amyloid), their translation to the clinic has not provided the expected results. Increasing evidences have demonstrated the presence of aggregates of TDP-43 (TAR DNA binding protein 43) in the postmortem brains of patients diagnosed with AD. The present research is focused on of the study of the pathological role of TDP-43 in AD. For this purpose, immortalized lymphocytes samples from patients diagnosed with different severity of sporadic AD were used and the TDP-43 pathology was analyzed against controls, looking for differences in their fragmentation, phosphorylation and cellular location using Western blot and immunocytochemical techniques. The results revealed an increase in TDP-43 fragmentation, as well as increased phosphorylation and aberrant localization of TDP-43 in the cytosolic compartment of lymphocytes of patients diagnosed with severe AD. Moreover, a fragment of approximately 25 KD was found in the extracellular medium of cells derived from severe AD individuals that seem to have prion-like characteristics. We conclude that TDP-43 plays a key role in AD pathogenesis and its cell to cell propagation.
... Moreover, the influence of these analogs on microglial morphology and function, along with their impact on histone H3 expression and methylation, suggests their broader implications in neuroinflammatory processes mediated in a wide range of interactions [73,112,113]. By modulating microglial behavior and epigenetic regulation, these analogs may exert neuroprotective effects, potentially attenuating the progression of debilitating disorders [114][115][116][117]. The multifaceted actions of these analogs on both the immune response and epigenetic regulation highlight their promise as a novel class of compounds for addressing the complex pathophysiological mechanisms underlying various neuropsychiatric and neurologic conditions [118][119][120]. ...
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The central nervous system (CNS) is the final frontier in drug delivery because of the blood-brain barrier (BBB), which poses significant barriers to the access of most drugs to their targets. Kynurenic acid (KYNA), a tryptophan (Trp) metabolite, plays an important role in behavioral functions, and abnormal KYNA levels have been observed in neuropsychiatric conditions. The current challenge lies in delivering KYNA to the CNS owing to its polar side chain. Recently, C-3 side chain-modified KYNA analogs have been shown to cross the BBB; however, it is unclear whether they retain the biological functions of the parent molecule. This study examined the impact of KYNA analogs, specifically, SZR-72, SZR-104, and the newly developed SZRG-21, on behavior. The analogs were administered intracerebroventricularly (i.c.v.), and their effects on the motor domain were compared with those of KYNA. Specifically, open-field (OF) and rotarod (RR) tests were employed to assess motor activity and skills. SZR-104 increased horizontal exploratory activity in the OF test at a dose of 0.04 µmol/4 µL, while SZR-72 decreased vertical activity at doses of 0.04 and 0.1 µmol/4 µL. In the RR test, however, neither KYNA nor its analogs showed any significant differences in motor skills at either dose. Side chain modification affects affective motor performance and exploratory behavior, as the results show for the first time. In this study, we showed that KYNA analogs alter emotional components such as motor-associated curiosity and emotions. Consequently, drug design necessitates the development of precise strategies to traverse the BBB while paying close attention to modifications in their effects on behavior.
... This shift aligns with broader discourse on the complexity and multifaceted nature of memory and learning processes [29][30][31]. These findings suggest that comprehending the neural correlates and molecular mechanisms underlying anxiety disorders, particularly in the context of fear acquisition and extinction, opens new avenues for therapeutic interventions. ...
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Neurodegeneration is a major problem in neuroscience and medicine as it causes and worsens many neurological and psychiatric disorders. It involves gradual loss of neurons at different levels of the brain, affecting cognition, emotion, behavior, consciousness, and attention. Understanding the causes and consequences of neurodegeneration is crucial for identifying the risk factors, biomarkers, and treatments. However, the current therapies are mostly symptomatic and ineffective. Therefore, new and innovative methods, such as noninvasive brain stimulation (NIBS), are needed to modulate brain activity and plasticity in a safe and reversible manner. This field is rapidly developing, with a focus on exploring new clinical applications, mechanisms, and combinations of NIBS and drugs. This special issue covers the latest progress and challenges in the study of neurodegeneration in cognitive impairment and mood disorders from the experimental, clinical, and translational perspectives. It addresses the complexity and diversity of these conditions, the lack of disease-modifying treatments, the ethical and practical issues of conducting research in vulnerable and diverse populations, the integration and interpretation of data from multiple sources and modalities, and the development and validation of novel methods such as NIBS, artificial intelligence, and drug repurposing. Collaborative efforts among various stakeholders are needed to improve our knowledge and treatment of neurodegeneration underlying cognitive impairment and mood disorders.
... Moreover, the influence of these analogs on microglial morphology and function, along with their impact on histone H3 expression and methylation, suggests their broader implications in neuroinflammatory processes mediated by brain-heart interactions [73,112,113]. By modulating microglial behavior and epigenetic regulation, these analogs may exert neuroprotective effects, potentially attenuating the progression of debilitating disorders [114][115][116][117]. The multifaceted actions of these analogs on both the immune response and epigenetic regulation highlight their promise as a novel class of compounds for addressing the complex pathophysiological mechanisms underlying various neuropsychiatric and neurologic conditions [118][119][120]. ...
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The central nervous system (CNS) is the final frontier in drug delivery because of the blood-brain barrier (BBB), which poses significant barriers to the access of most drugs to their targets. Kynurenic acid (KYNA), a tryptophan (Trp) metabolite, plays an important role in behavioral functions and abnormal KYNA levels have been observed in neuropsychiatric conditions. The current challenge lies in delivering KYNA to the CNS owing to its polar side chain. Recently, C-3 side chain modified KYNA analogs have been shown to cross the BBB; however, it is unclear whether they retain the biological functions of the parent molecule. This study examined the impact of KYNA analogs, specifically SZR-72, SZR-104, and the newly developed SZRG-21, on behavior. The analogs were administered intracerebroventricularly (i.c.v.), and their effects on the motor domain were compared with those of KYNA. Specifically, open field (OF) and rotarod (RR) tests were employed to assess motor activity and skills. SZR-104 increased horizontal exploratory activity in the OF test at a dose of 0.04 μmol/4 μL, while SZR-72 decreased vertical activity at doses of 0.04 and 0.1 μmol/4 μL. In the RR test, however, neither KYNA nor its analogs showed any significant differences in motor skills at either dose. Side chain modification affects affective motor performance and exploratory behavior, as the results show for the first time. In this study, we showed that KYNA analogs alter emotional components such as motor-associated curiosity and emotions. Consequently, drug design necessitates the development of precise strategies to traverse the BBB while paying close attention to modifications in their effects on behavior.
... These complex processes are controlled by a cortico-subcortical network involving the amygdala, which works together with prefrontal regions to form emotional memories [13]. The proper regulation of emotional responses to potential threats is pivotal in maintaining mental well-being, as disruptions in emotion regulation can contribute to trauma-related disorders, such as anxiety and mood disorders [7,18,[24][25][26][27][28][29][30][31][32]. ...
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Fear extinction is a phenomenon that involves a gradual reduction in conditioned fear responses through repeated exposure to fear-inducing cues. Functional brain connectivity assessments , such as functional magnetic resonance imaging (fMRI), provide valuable insights into how brain regions communicate during these processes. Stress, a ubiquitous aspect of life, influences fear learning and extinction by changing the activity of the amygdala, prefrontal cortex, and hippocampus, leading to enhanced fear responses and/or impaired extinction. Glucocorticoid receptors (GRs) are key to the stress response and show a dual function in fear regulation: while they enhance the consolidation of fear memories, they also facilitate extinction. Accordingly, GR dysregulation is associated with anxiety and mood disorders. Recent advancements in cognitive neuroscience underscore the need for a comprehensive understanding that integrates perspectives from the molecular, cellular, and systems levels. In particular, neuropharmacology provides valuable insights into neurotrans-mitter and receptor systems, aiding the investigation of mechanisms underlying fear regulation and potential therapeutic targets. A notable player in this context is cortisol, a key stress hormone, which significantly influences both fear memory reconsolidation and extinction processes. Gaining a thorough understanding of these intricate interactions has implications in terms of addressing psychiatric disorders related to stress. This review sheds light on the complex interactions between cognitive processes, emotions, and their neural bases. In this endeavor, our aim is to reshape the comprehension of fear, stress, and their implications for emotional well-being, ultimately aiding in the development of therapeutic interventions.
... Cognitive impairment in BD patients is associated with metabolic factors, gene polymorphisms, brain structural and functional changes, and neuroinflammation [46]. Emotions can improve or impair cognitive performance [47], and it is important to understand the functional interplay between the central and autonomic nervous systems and to elucidate how emotions are integrated into executive functions in neuropsychiatric diseases [48,49]. This is crucial for regulating physiological processes and maintaining homeostasis, with the prefrontal cortex playing a key role [50,51]. ...
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Mitochondrial dysfunction is an important cellular hallmark of aging and neurodegeneration. Platelets are a useful model to study the systemic manifestations of mitochondrial dysfunction. To evaluate the age dependence of mitochondrial parameters, citrate synthase activity, respiratory chain complex activity, and oxygen consumption kinetics were assessed. The effect of cognitive impairment was examined by comparing the age dependence of mitochondrial parameters in healthy individuals and those with neuropsychiatric disease. The study found a significant negative slope of age-dependence for both the activity of individual mitochondrial enzymes (citrate synthase and complex II) and parameters of mitochondrial respiration in intact platelets (routine respiration, maximum capacity of electron transport system, and respiratory rate after complex I inhibition). However, there was no significant difference in the age-related changes of mitochondrial parameters between individuals with and without cognitive impairment. These findings highlight the potential of measuring mitochondrial respiration in intact platelets as a means to assess age-related mitochondrial dysfunction. The results indicate that drugs and interventions targeting mitochondrial respiration may have the potential to slow down or eliminate certain aging and neurodegenerative processes. Mitochondrial respiration in platelets holds promise as a biomarker of aging, irrespective of the degree of cognitive impairment.
... Emotion dysregulation is considered a crucial aspect of depression, as emotions have the ability to influence behavior [2]. Thus, it is essential to comprehend the neural mechanisms behind the impaired inhibitory control, which is prevalent in several psychopathologies and mood disorders, including depression, anxiety, and fear conditioning [3,4]. Emotion regulation has been identified as a central process in both the research and treatment of depression [5]. ...
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Depression is a complex clinical disorder associated with poor outcomes. Electroacupuncture (EA) has been demonstrated to have an important role in both clinical and pre-clinical depression investigations. Evidence has suggested that the P2X7 receptor (P2X7R), NLRP3, and IL-1β play an important role in depressive disorder. Our study is aimed at exploring the role of EA in alleviating depression-like behaviors in rats. We therefore investigated the effects of EA on the prefrontal cortex and liver of rats subjected to chronic unpredictable mild stress (CUMS) through behavior tests, transmission electron microscopy, Nissl staining, HE staining, immunohistochemistry and Western blotting. Five weeks after exposure to CUMS, Sprague-Dawley (SD) rats showed depression-like behavior. Three weeks after treatment with brilliant blue G (BBG) or EA, depressive symptoms were significantly improved. Liver cells and microglia showed regular morphology and orderly arrangement in the BBG and EA groups compared with the CUMS group. Here we show that EA downregulated P2X7R/NLRP3/IL-1β expression and relieved depression-like behavior. In summary, our findings demonstrated the efficacy of EA in alleviating depression-like behaviors induced by CUMS in rats. This suggests that EA may serve as an adjunctive therapy in clinical practice, and that P2X7R may be a promising target for EA intervention on the liver–brain axis in treatment of depression.
... The current consensus conference did not recommend any specific neuropsychological test that could be used with this purpose; however, it is important to mention that impulse control abilities could be measured using tests such as the Stroop test [88], the Hayling test [89,90], or the computerized go/no-go [91] or stop signal [92] tests. The affective variant of the stop signal task is also particularly interesting as it can reveal a difficulty in inhibition only when an emotional component in the stimuli is present [93]. Similarly, the theory of mind ability could be measured by means of the Story Empathy Task (SET, [94]), the Theory of Mind Inventory [95] or the social cognition battery [96]. ...
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Idiopathic and acquired pedophilia are two different disorders with two different etiologies. However, the differential diagnosis is still very difficult, as the behavioral indicators used to discriminate the two forms of pedophilia are underexplored, and clinicians are still devoid of clear guidelines describing the clinical and neuroscientific investigations suggested to help them with this difficult task. Furthermore, the consequences of misdiagnosis are not known, and a consensus regarding the legal consequences for the two kinds of offenders is still lacking. The present study used the Delphi method to reach a global consensus on the following six topics: behavioral indicators/red flags helpful for differential diagnosis; neurological conditions potentially leading to acquired pedophilia; neuroscientific investigations important for a correct understanding of the case; consequences of misdiagnosis; legal consequences; and issues and future perspectives. An international and multidisciplinary board of scientists and clinicians took part in the consensus statements as Delphi members. The Delphi panel comprised 52 raters with interdisciplinary competencies, including neurologists, psychiatrists, neuropsychologists, forensic psychologists, expert in ethics, etc. The final recommendations consisted of 63 statements covering the six different topics. The current study is the first expert consensus on a delicate topic such as pedophilia. Important exploitable consensual recommendations that can ultimately be of immediate use by clinicians to help with differential diagnosis and plan and guide therapeutic interventions are described, as well as future perspectives for researchers.
... Also, regarding the mechanism that underline neurocognitive changes in CHC patients, a review article suggested impairments in emotional learning, memory and how this ability, together with deficient inhibitory control, are core factors in different psychopathologies. As, these impairments caused dysfunctional behaviours, such as deficit in action control and motor inhibition, that are associated with psychopathological and psychiatric conditions, which are characterized by severe impulsivity problems that can determine significant impairment or distress (due to poor regulation and capacity of control, which can be intensified in the presence of emotional stimuli) and result in neurocognitive change [8]. ...
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Background Hepatitis C virus (HCV) infection is associated with psychiatric and cognitive dysfunctions. We aimed to investigate depression, anxiety, and cognitive function of chronic hepatitis C (CHC) patients before and after treatment with direct-acting antivirals (DAAs). Forty CHC patients (20 non-cirrhotic and 20 cirrhotic) who had undergone DAA treatment in our outpatient clinic and ten controls. We administered the Hospital Anxiety and Depression questionnaires to measure the anxiety and depression symptoms and the Cognitive Abilities Screening Instruments (CASI) to measure the cognitive function at the beginning and 3 months after the end of the treatment. Results Sustained virological response (SVR) was achieved in all patients. Post-treatment anxiety and depression scores showed a significant improvement than pre-treatment ones in CHC patients. Regarding CASI, before and after the treatment, a statistical significance was found in short-term memory ( P = 0.001), concentration ( P = 0.033), abstract thinking and judgment ( P = 0.024), total ( P = 0.001) in non-cirrhotic, Also, an improvement was seen in long-term memory ( P = 0.015), short-term memory ( P < 0.001), concentration ( P = 0.024) and total ( P = 0.01) in cirrhotic. However, these changes were still impaired in post-treated cirrhotic compared to controls. Conclusions CHC patients' anxiety, depression, and cognitive function partially improved after DAA therapy. Besides, improving the status of CHC, reversibility of cognitive dysfunction in non-cirrhotic patients may indicate the importance of treatment in early stages of liver disease.
... Recent observations reported differential impairment of the core aspects of social cognitive processing in patients with MS [15]. Moreover, alterations of learning and memory processes, together with typical dysfunctional behaviours, such as deficits in action control and motor inhibition, have been found to be core factors in different neurodegenerative disorders [16]. Other aspects, relatively less evaluated in MS, such as altered emotion perception, can contribute to cognitive dysfunction [17]. ...
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Cognitive impairment (CI) is a core feature of multiple sclerosis (MS) and affects up to 65% of patients in every phase of the disease, having a deep impact on all aspects of patients’ lives. Cognitive functions most frequently involved include information processing speed, learning and memory, visuospatial abilities, and executive function. The precise pathogenetic mechanisms underpinning CI in MS are still largely unknown, but are deemed to be mainly related to pathological changes in lesioned and normal-appearing white matter, specific neuronal grey matter structures, and immunological alterations, with particular impact on synaptic transmission and plasticity. Moreover, much research is needed on therapeutic strategies. Small to moderate efficacy has been reported for disease-modifying therapies, particularly high-efficacy drugs, and symptomatic therapies (dalfampridine), while the strongest benefit emerged after cognitive training. The present narrative review provides a concise, updated overview of more recent evidence on the prevalence, profile, pathogenetic mechanisms, and treatment of CI in people with MS. CI should be screened on a regular basis as part of routine clinical assessments, and brief tools are now widely available (such as the Symbol Digit Modalities Test). The main goal of cognitive assessment in MS is the prompt implementation of preventive and treatment interventions.
... Recent advancements in neuroscience have enabled researchers to probe the brain in larger regions, at the cellular level, and with increased receptor specificity [2][3][4][5][6]. Research is focused on finding scientific frameworks for understanding the neuropathophysiology of mental illnesses, exploring the molecular regulation of higher-order neural circuits and neuropathological alterations, which may lead to prefrontal cortex (PFC) dysfunction, eliciting the symptoms of mental illnesses [7][8][9][10][11][12][13]. The deficit in control and motor inhibition [14][15][16], in motor imagery or in the suppression of ongoing action [17], or in emotion perception, reactivity, and regulation [18][19][20], which depend on aberrant neural activity in the PFC associated with serious impulsivity problems, are characterized in neuropsychiatric disorders. ...
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“To learning much inclined, who went to see the Elephant (though all of them were blind) that each by observation might satisfy the mind” [...]
... Recently, reporting guidelines established by European experts on therapeutic repetitive transcranial magnetic stimulation (rTMS) and other literature have recommended rTMS as a therapeutic strategy for several neurological and psychiatric disorders [57] and regulation of the nodes in the prefrontal cortex involved in the control of fear responses [58]. Multiple high-frequency rTMS sessions over the dorsolateral prefrontal cortex (DLPFC) may improve executive function in patients with PD [59]. ...
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Background: Delayed neuropsychiatric syndrome (DNS) is characterized by motor dysfunction after acute carbon monoxide (CO) poisoning. We examined the relationship between dopamine transporter (DAT) loss using kit-based Tc-99m-TRODAT-1 (DAT single-photon emission-computed tomography (SPECT) radioligand) and globus pallidus necrosis on MRI, DAT availability before and after hyperbaric oxygen therapy (HBOT), and feasibility of Tc-99m-TRODAT-1 as an index for parkinsonian syndrome in CO poisoning. Methods: Twenty-one CO-intoxicated patients (mean ± SD age, 38.6 ± 11.4; range, 20-68 years) with DNS underwent Tc-99m-TRODAT-1 SPECT and MRI before HBOT and follow-up Tc-99m-TRODAT-1 SPECT to assess DAT recovery. Neurological examinations for Parkinsonism were performed after development of DNS. Results: Over 70% (15/21) of DNS patients showed globus pallidus necrosis on MRI. Significantly lower bilateral striatal DAT availability was associated with globus pallidus necrosis (p < 0.005). Moreover, 68.4% (13/19) of DNS subjects with Parkinsonian syndrome had lower bilateral striatal DAT availability vs. non-parkinsonian subjects pre- or post-HBOT. The SURs for both striata increased by ~11% post-HBOT in the Parkinsonian group; however, the left striatum presented a significantly higher DAT recovery rate than the right (*** p < 0.005). Conclusions: Coupled Tc-99m TRODAT-1 SPECT and MRI could assist evaluation of Parkinsonism risk and indicate DAT availability after HBOT in CO-poisoned patients with DNS.
... 5 In addition, recent evidence from studies on action control conducted on healthy individuals supported a causal role of dopamine in action control, and others addressed how PD is accompanied by impairments in covert cognitive processes. 6,7 Still, other studies investigated underlying goaldirected motor functioning (e.g., action planning, conflict adaptation, motor inhibition) 8,9 and how dopaminergic medication may modulate these action control components. ...
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Background: Brain-derived neurotrophic factor (BDNF) is essential for the development of dopaminergic neurons in the substantia nigra. Objectives: To investigate the level of BDNF among Parkinson's disease (PD) subjects and the influence of depression on BDNF levels. Material and methods: A total of 1920 subjects were included in the analysis; of these, 1034 had PD and 886 were healthy controls. A thorough literature search up to May 2022 was conducted. The mean difference (MD) of BDNF levels and 95% confidence intervals (95% CIs) were calculated with random or fixed effects models. Results: Compared to healthy controls, levels of BDNF were significantly lower in patients with PD (MD = -1.60, 95% CI (-2.49, -0.70), p < 0.001). Patients with PD and depression had significantly lower levels of BDNF (MD = -3.39, 95% CI (-5.55, -1.23), p = 0.002), as well as those with PD without depression (MD = -0.80, 95% CI (-1.56, -0.03), p = 0.04). However, there was no discernible change in BDNF levels (MD = -0.82, 95% CI (1.75, 0.10), p = 0.08) between the participants with PD and depression compared to the PD patients alone. Conclusion: Compared with healthy controls, BDNF levels were significantly lower in the subjects with PD combined with depression, and PD without depression. However, there was no discernible difference in BDNF levels between subjects with PD with depression compared to those with PD without depression.
... Recently, some researches on depression are focused on the relationship between the molecular regulation of neural networks and neuropathological changes, and how this may cause to PFC dysfunction and to the symptoms and features of psychiatric diseases (Tanaka et al. 2022b). The deficit in control and motor inhibition (Battaglia et al. 2022a), also in motor imagery or in the suppression of on-going action, which is based on abnormal neural activity in the PFC, are characterized by psychiatric conditions including major depression (Tanaka et al. 2022b;Battaglia et al. 2022bBattaglia et al. , 2021. It is also stated that neurodevelopmental processes that interact with the immune system and epigenetics play a role in the pathogenesis (Gałecka et al. 2021;Tanaka et al. 2022a). ...
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The kynurenine pathway (KP) and inflammation are substantial in depression pathogenesis. Although there is a crosstalk between the KP, inflammation, and neurotrophic factors, few studies examine these topics together. Novel medications may be developed by clarifying dysregulations related to inflammation, KP, and neurotrophic factors in treatment-resistant depression (TRD). We aimed to evaluate the serum levels of KP metabolites, proinflammatory biomarkers, and brain-derived neurotrophic factor (BDNF) in healthy controls (HC) and the patients with TRD whose followed up with three different treatments. Moreover, the effect of electroconvulsive therapy (ECT) and repetitive transcranial magnetic stimulation (rTMS) on biomarkers was investigated. Study groups comprised a total of 30 unipolar TRD patients consisting of three separate patient groups (ECT = 8, rTMS = 10, pharmacotherapy = 12), and 9 HC. The decision to administer only pharmacotherapy or ECT/rTMS besides pharmacotherapy was given independently of this research by psychiatrists. Blood samples and symptom scores were obtained three times for patients. At baseline, quinolinic acid (QUIN) was higher in the patients with TRD compared to HC, whereas picolinic acid (PIC), PIC/QUIN, and PIC/3-hydroxykynurenine were lower. Baseline interleukin-6 (IL-6), and high-sensitivity C-reactive protein (hsCRP) were higher in nonresponders and non-remitters. ECT had an acute effect on cytokines. In the rTMS group, tumor necrosis factor-α (TNF-α) decreased in time. PIC, QUIN, and aminocarboxymuconate-semialdehyde decarboxylase (ACMSD) enzyme may play a role in TRD pathogenesis, and have diagnostic potential. rTMS and ECT have modulatory effects on low-grade inflammation seen in TRD. Baseline inflammation severity is predictive in terms of response and remission in depression.
... Furthermore, the intentional neglect of adaptive procees necessary for memory functioning and functional alterations in the PFC affects the memory and learning abilities of psychiatric and brain-damaged patients. The human ventromedial PFC is responsible for the capacity of associative learning [130][131][132]. Hypoactivation in the ventromedial PFC with hyperactivation in the dorsal anterior cingulate cortex are reported in patients with PTSD and SCZ [133,134]. ...
Article
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Nearly half a century has passed since the discovery of cytoplasmic inheritance of human chloramphenicol resistance. The inheritance was then revealed to take place maternally by mitochondrial DNA (mtDNA). Later, a number of mutations in mtDNA were identified as a cause of severe inheritable metabolic diseases with neurological manifestation, and the impairment of mitochondrial functions has been probed in the pathogenesis of a wide range of illnesses including neurodegenerative diseases. Recently, a growing number of preclinical studies have revealed that animal behaviors are influenced by the impairment of mitochondrial functions and possibly by the loss of mitochondrial stress resilience. Indeed, as high as 54% of patients with one of the most common primary mitochondrial diseases, mitochondrial encephalomyopathy with lactic acidosis and stroke-like episodes (MELAS) syndrome, present psychiatric symptoms including cognitive impairment, mood disorder, anxiety, and psychosis. Mitochondria are multifunctional organelles which produce cellular energy and play a major role in other cellular functions including homeostasis, cellular signaling, and gene expression, among others. Mitochondrial functions are observed to be compromised and to become less resilient under continuous stress. Meanwhile, stress and inflammation have been linked to the activation of the tryptophan (Trp)-kynurenine (KYN) metabolic system, which observably contributes to the development of pathological conditions including neurological and psychiatric disorders. This review discusses the functions of mitochondria and the Trp-KYN system, the interaction of the Trp-KYN system with mitochondria, and the current understanding of the involvement of mitochondria and the Trp-KYN system in preclinical and clinical studies of major neurological and psychiatric diseases.
... As stated in the diagnostic criteria, functional impairment is typically the leading cause of admission [3], but it typically fades and becomes less germane during routine in clinical practice. Recent evidence suggests that ADHD-related emotional dysregulation symptoms (poor management of anger and irritability), fear learning [4] and difficulties in motor inhibition [5] which are thought to be related to some neuroanatomical [6] and neurochemical [7] developmental processes, could impact functioning [8]. Besides, functional impairment in ADHD has attracted considerable interest in literature, which suggests that its trends are not always in parallel to symptoms [9,10]. ...
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Background: Recent guidelines emphasize the importance of functional outcomes in children with Attention-Deficit/Hyperactivity Disorder (ADHD). Here, we assess the functional outcomes of the oral delivery system of osmotic release methylphenidate (OROS-MPH) and atomoxetine (ATX) from the retrospective review of the chart for the last two years in the clinic. Results: Linear mixed-effects models were performed with outcome measures of difference in ADHD symptoms and functional impairment. After 9-12 weeks, OROS-MPH and ATX were statistically equivalent for total Weiss Functıonal Impairment Rating Scale – Parent Report (WFIRS-P) scores (difference in slope is β= 0.004, p=1.000). However, OROS-MPH was superior to ATX in terms of school domain (difference in slope is β = 0.139 p <0.001); ATX was superior in the family domain (slope difference in slope is β = 0.103, p <0.001). The other domains of functioning both were not responsive to pharmacotherapy and were similar between the two medications. Conclusions: Optimal management should monitor functional progress in ADHD beyond the core symptoms. As expected, ADHD medications provide a distinct pattern of functional improvement. Pharmacotherapy alone offers promising and reliable outcomes to improve school and family functions in ADHD. Some functional improvements did not respond to the medication; therefore, many of the techniques derived from behavioral interventions should be considered.
... Furthermore, functional alterations in the PFC affects the memory and learning abilities of psychiatric and brain-damaged patients. The human ventromedial PFC is responsible for the capacity of associative learning [122,123] Hypoactivation in the ventromedial PFC with hyperactivation in the dorsal anterior cingulate cortex are reported in patients with PTSD and SCZ [124,125]. These evidence suggests that PFC dysfunctions cause impairment of aversive learning and emotional memory circuits, which might be transversal across many psychiatric disorders in humans. ...
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Nearly half a century has passed since the discovery of cytoplasmic inheritance of human chloramphenicol resistance. The inheritance was then revealed to take place maternally by mito-chondrial DNA (mtDNA). Later, a number of mutations in mtDNA were identified as a cause of severe inheritable metabolic diseases with neurological manifestation, and the impairment of mito-chondrial functions has been probed in the pathogenesis of a wide range of illnesses including neu-rodegenerative diseases. Recently growing number of preclinical studies has revealed that animal behaviors are influenced by the impairment of mitochondrial functions and possibly by the loss of mitochondrial stress resilience. Indeed, as high as 54% of patients with one of the most common primary mitochondrial diseases, mitochondrial encephalomyopathy with lactic acidosis and stroke-like episodes (MELAS) syndrome, present psychiatric symptoms including cognitive impairment, mood disorder, anxiety, and psychosis. Mitochondria are multifunctional organelles which produce cellular energy and play a major role in other cellular functions including homeostasis, cellular sig-naling, and gene expression, among other. Mitochondrial functions are observed to be compromised and to become less resilient under continuous stress. Meanwhile, stress and inflammation have been linked to the activation of the tryptophan (Trp)-kynurenine (KYN) metabolic system, which observably contributes to development of pathological conditions including neurological and psychiatric disorders. This narrative review discusses the functions of mitochondria and the Trp-KYN system, the interaction of the Trp-KYN system with mitochondria, and the current understanding of the involvement of mitochondria and the Trp-KYN system in preclinical and clinical studies of major neurological and psychiatric diseases.
... According to the literature, it is common for ADHD to present problems in maintaining attention, and therefore, when performing a task, this will impact the correctness and the reaction time. The theme of our video game, driving a car without distractions, was deliberately chosen with the intention of avoiding introducing emotional biases that could affect reaction times [11]. No rewarding gamification elements were introduced to minimize the risk for video game addiction [59]. ...
Article
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Symptoms of Attention Deficit Hyperactivity Disorder (ADHD) include excessive activity, difficulty sustaining attention, and inability to act in a reflective manner. Early diagnosis and treatment of ADHD is key but may be influenced by the observation and communication skills of caregivers, and the experience of the medical professional. Attempts to obtain additional measures to support the medical diagnosis, such as reaction time when performing a task, can be found in the literature. We propose an information recording system that allows to study in detail the behavior shown by children already diagnosed with ADHD during a car driving video game. We continuously record the participants’ activity throughout the task and calculate the error committed. Studying the trajectory graphs, some children showed uniform patterns, others lost attention from one point onwards, and others alternated attention/inattention intervals. Results show a dependence between the age of the children and their performance. Moreover, by analyzing the positions by age over time using clustering, we show that it is possible to classify children according to their performance. Future studies will examine whether this detailed information about each child’s performance pattern can be used to fine-tune treatment.
... Moreover, Gray (17,18) believed that cognition and emotion are strongly integrated and inseparable in the process of information processing (19). A meta-analysis of inhibitory control demonstrated that several brain areas have been associated with the mechanisms underlying inhibitory control, with a network involving left and right inferior frontal gyrus (IFG) dorsolateral pre-frontal cortex (dlPFC), anterior cingulate (ACC) (20). ...
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Background Impairment of interference control ability may reflect a more general deficit in executive functioning, and lead to an increase in internal-externalized problems such as impulsivity, which has been reported in deaf children. However, few researches have examined the neural mechanism of this impairment. Methods This study applied the electroencephalogram (EEG) technique to investigate the interference control ability in 31 deaf children and 28 hearing controls with emotional face-word stroop task. Results Results from behavioral task showed that deaf children exhibited lower accuracy compared to hearing controls. As for EEG analysis, reduced activation of ERP components in N1 and enhanced activation of ERP components in N450 have been found in deaf children. Besides, incongruent condition elicited larger N450 than congruent condition. Furthermore, for brain oscillation, alpha band (600–800 ms) revealed a reduced desynchronization in deaf children, while theta band (200–400 ms) revealed an enhanced synchronization in deaf children and incongruent condition, which were in line with ERP components. Conclusion The present findings seem to indicate that the deficit during emotional interference control ability among deaf children might be due to the impaired attention allocation ability and emotional cognitive monitoring function during emotional conflict detection process. Consequently, reduced N1 and enhanced N450 might be due to early attention impairment causing more effort of deaf children later in emotional cognitive monitoring.
... By accounting for individual differences, we will be able to make better inferences in psychopathology and their causal links to neurobiology. The role of the emotional content in response inhibition is not clear [53] and we hope our findings will add on to this literature on evidence accumulation studies. ...
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The current study evaluated the impact of task-relevant emotion on inhibitory control while focusing on midline cortical regions rather than brain asymmetry. Single-trial time-frequency analysis of electroencephalography recordings linked with response execution and response inhibition was done while thirty-four participants performed the emotion modulated stop-signal task. To evaluate individual differences across decision-making processes involved in inhibitory control, a hierarchical drift-diffusion model was used to fit data from Go-trials for each of the 34 participants. Response threshold in the early processing stage for happy and disgust emotions could be distinguished from the later processing stage at the mid-parietal and mid-frontal regions, respectively, by the single-trial power increments in low frequency (delta and theta) bands. Beta desynchronization in the mid-frontal region was specific for differentiating disgust from neutral emotion in the early as well as later processing stages. The findings are interpreted based on the influence of emotional stimuli on early perceptual processing originating as a bottom-up process in the mid-parietal region and later proceeding to the mid-frontal region responsible for cognitive control processing, which resulted in enhanced inhibitory performance. The results show the importance of mid-frontal and mid-parietal regions in single-trial dynamics of inhibitory control processing.
... It is worthwhile to understand the neural bases of gaze direction and gaze-cueing and which contextual factors, such as facial emotional expressions, can modulate the subsequent brain activations. In turn, this helps with understanding the underlying processes causing impairments in social cognition and social functioning that are associated with various psychiatric, neurological and neurodegenerative illnesses [36][37][38][39][40]. ...
Article
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The ability to adaptively follow conspecific eye movements is crucial for establishing shared attention and survival. Indeed, in humans, interacting with the gaze direction of others causes the reflexive orienting of attention and the faster object detection of the signaled spatial location. The behavioral evidence of this phenomenon is called gaze-cueing. Although this effect can be conceived as automatic and reflexive, gaze-cueing is often susceptible to context. In fact, gaze-cueing was shown to interact with other factors that characterize facial stimulus, such as the kind of cue that induces attention orienting (i.e., gaze or non-symbolic cues) or the emotional expression conveyed by the gaze cues. Here, we address neuroimaging evidence, investigating the neural bases of gaze-cueing and the perception of gaze direction and how contextual factors interact with the gaze shift of attention. Evidence from neuroimaging, as well as the fields of non-invasive brain stimulation and neurologic patients, highlights the involvement of the amygdala and the superior temporal lobe (especially the superior temporal sulcus (STS)) in gaze perception. However, in this review, we also emphasized the discrepancies of the attempts to characterize the distinct functional roles of the regions in the processing of gaze. Finally, we conclude by presenting the notion of invariant representation and underline its value as a conceptual framework for the future characterization of the perceptual processing of gaze within the STS.
... Meanwhile, data from the oldest woman and data from a woman with AD were selected for testing to test the generalizability of the model. The relevance, strength, and valence of emotional input, as well as the impacted component of motor control of the face, are crucial considerations, according to Battalia et al. [68]. All of this evidence suggests that understanding how emotion is integrated into key executive functions such as inhibitory control is crucial not only for cognitive neuroscience but also for improving neurocognitive models of psychopathology. ...
Article
Visual perception is an important part of human life. In the context of facial recognition, it allows us to distinguish between emotions and important facial features that distinguish one person from another. However, subjects suffering from memory loss face significant facial processing problems. If the perception of facial features is affected by memory impairment, then it is possible to classify visual stimuli using brain activity data from the visual processing regions of the brain. This study differentiates the aspects of familiarity and emotion by the inversion effect of the face and uses convolutional neural network (CNN) models (EEGNet, EEGNet SSVEP (steady-state visual evoked potentials), and DeepConvNet) to learn discriminative features from raw electroencephalography (EEG) signals. Due to the limited number of available EEG data samples, Generative Adversarial Networks (GAN) and Variational Autoencoders (VAE) are introduced to generate synthetic EEG signals. The generated data are used to pretrain the models, and the learned weights are initialized to train them on the real EEG data. We investigate minor facial characteristics in brain signals and the ability of deep CNN models to learn them. The effect of face inversion was studied, and it was observed that the N170 component has a considerable and sustained delay. As a result, emotional and familiarity stimuli were divided into two categories based on the posture of the face. The categories of upright and inverted stimuli have the smallest incidences of confusion. The model’s ability to learn the face-inversion effect is demonstrated once more.
... One study aimed to genotype 6 polymorphisms of the CNR1 gene and the 385C>A SNP of the FAAH gene in former heroin addicts and their corresponding controls distinguishing between ethnicities (Caucasians, Hispanics, African Americans and Asians). Long repeats of the triplet polymorphism of CNR1 18087-18131(TAA) [8][9][10][11][12][13][14][15][16][17] were significantly associated with vulnerability to develop heroin addiction. Conversely, the allele 1359A and the genotype 1359AA of CNR1 were associated with a protective effect, particularly in Caucasians. ...
Article
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Despite substance use disorders (SUD) being one of the leading causes of disability and mortality globally, available therapeutic approaches remain ineffective. The difficulty in accurately characterizing the neurobiological mechanisms involved with a purely qualitative diagnosis is an obstacle to improving the classification and treatment of SUD. In this regard, identifying central and peripheral biomarkers is essential to diagnosing the severity of drug dependence, monitoring therapeutic efficacy, predicting treatment response, and enhancing the development of safer and more effective pharmacological tools. In recent years, the crucial role that the endocannabinoid system (ECS) plays in regulating the reinforcing and motivational properties of drugs of abuse has been described. This has led to studies characterizing ECS alterations after exposure to various substances to identify biomarkers with potential diagnostic, prognostic, or therapeutic utility. This review aims to compile the primary evidence available from rodent and clinical studies on how the ECS components are modified in the context of different substance-related disorders, gathering data from genetic, molecular, functional, and neuroimaging experimental approaches. Finally, this report concludes that additional translational research is needed to further characterize the modifications of the ECS in the context of SUD, and their potential usefulness in the necessary search for biomarkers.
... Future investigations to identify characteristic structures related to (A) higher cortical functions will include the prefrontal cortex and (B) learning and emotions will include the hippocampus and the amygdala. Future work will include measurement of inhibitory control [95], mediofrontal negativity [96], and other additional variables likely to be impaired in men with FXS. ...
Article
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Multiple lines of evidence suggest that a deficiency of Fragile X Mental Retardation Protein (FMRP) mediates dysfunction of the metabotropic glutamate receptor subtype 5 (mGluR5) in the pathogenesis of fragile X syndrome (FXS), the most commonly known single-gene cause of inherited intellectual disability (ID) and autism spectrum disorder (ASD). Nevertheless, animal and human studies regarding the link between FMRP and mGluR5 expression provide inconsistent or conflicting findings about the nature of those relationships. Since multiple clinical trials of glutamatergic agents in humans with FXS did not demonstrate the amelioration of the behavioral phenotype observed in animal models of FXS, we sought measure if mGluR5 expression is increased in men with FXS to form the basis for improved clinical trials. Unexpectedly marked reductions in mGluR5 expression were observed in cortical and subcortical regions in men with FXS. Reduced mGluR5 expression throughout the living brains of men with FXS provides a clue to examine FMRP and mGluR5 expression in FXS. In order to develop the findings of our previous study and to strengthen the objective tools for future clinical trials of glutamatergic agents in FXS, we sought to assess the possible value of measuring both FMRP levels and mGluR5 expression in men with FXS. We aimed to show the value of measurement of FMRP levels and mGluR5 expression for the diagnosis and treatment of individuals with FXS and related conditions. We administered 3-[18F]fluoro-5-(2-pyridinylethynyl)benzonitrile ([18F]FPEB), a specific mGluR5 radioligand for quantitative measurements of the density and the distribution of mGluR5s, to six men with the full mutation (FM) of FXS and to one man with allele size mosaicism for FXS (FXS-M). Utilizing the seven cortical and subcortical regions affected in neurodegenerative disorders as indicator variables, adjusted linear regression of mGluR5 expression and FMRP showed that mGluR5 expression was significantly reduced in the occipital cortex and the thalamus relative to baseline (anterior cingulate cortex) if FMRP levels are held constant (F(7,47) = 6.84, p < 0.001).These findings indicate the usefulness of cerebral mGluR5 expression measured by PET with [18F]FPEB and FMRP values in men with FXS and related conditions for assessments in community facilities within a hundred-mile radius of a production center with a cyclotron. These initial results of this pilot study advance our previous study regarding the measurement of mGluR5 expression by combining both FMRP levels and mGluR5 expression as tools for meaningful clinical trials of glutamatergic agents for men with FXS. We confirm the feasibility of this protocol as a valuable tool to measure FMRP levels and mGluR5 expression in clinical trials of individuals with FXS and related conditions and to provide the foundations to apply precision medicine to tailor treatment plans to the specific needs of individuals with FXS and related conditions.
... By the time AD is diagnosed, the disease has progressed too far to be managed. Severely compromised brain function due to chronic pathological insults makes AD treatment more difficult, and a multitarget, rather than one-target treatment strategy, is required for this complex disease [27,28]. A favorable combination of decreased microglia-mediated neuroinflammation and enhanced Aβ clearance has been proposed as a promising therapeutic paradigm [29]. ...
Article
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Alzheimer’s disease (AD) is a progressive neurodegenerative disease with a multifactorial etiology. A multitarget treatment that modulates multifaceted biological functions might be more effective than a single-target approach. Here, the therapeutic efficacy of combination treatment using anti-Aβ antibody NP106 and curcumin analog TML-6 versus monotherapy was investigated in an APP/PS1 mouse model of AD. Our data demonstrate that both combination treatment and monotherapy attenuated brain Aβ and improved the nesting behavioral deficit to varying degrees. Importantly, the combination treatment group had the lowest Aβ levels, and insoluble forms of Aβ were reduced most effectively. The nesting performance of APP/PS1 mice receiving combination treatment was better than that of other APP/PS1 groups. Further findings indicate that enhanced microglial Aβ phagocytosis and lower levels of proinflammatory cytokines were concurrent with the aforementioned effects of NP106 in combination with TML-6. Intriguingly, combination treatment also normalized the gut microbiota of APP/PS1 mice to levels resembling the wild-type control. Taken together, combination treatment outperformed NP106 or TML-6 monotherapy in ameliorating Aβ pathology and the nesting behavioral deficit in APP/PS1 mice. The superior effect might result from a more potent modulation of microglial function, cerebral inflammation, and the gut microbiota. This innovative treatment paradigm confers a new avenue to develop more efficacious AD treatments.
... This is in line with research showing the use of TMS in modulating action inhibition in humans as measured by their performance on the stop-signal task through stimulation of the DLPFC [108]. Importantly, emotional stimuli processing in the brain can also disrupt inhibition performance, pointing to a possible interaction effect between cognition and affective symptoms reported by patients [109]. Indeed, experimental studies have shown how priming by negative emotionality affects motor responses through increases or decreases in corticospinal excitability [110]. ...
Article
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Major depressive disorder (MDD) and alcohol use disorder (AUD) are leading causes of disability, and patients are frequently affected by both conditions. This comorbidity is known to confer worse outcomes and greater illness severity. Repetitive transcranial magnetic stimulation (rTMS) is a non-invasive neuromodulation method that has demonstrated antidepressant effects. However, the study of rTMS for patients with MDD and commonly associated comorbidities, such as AUD, has been largely overlooked, despite significant overlap in clinical presentation and neurobiological mechanisms. This narrative review aims to highlight the interrelated aspects of the literature on rTMS for MDD and rTMS for AUD. First, we summarize the available evidence on the effectiveness of rTMS for each condition, both most studied through stimulation of the dorsolateral prefrontal cortex (DLPFC). Second, we describe common symptom constructs that can be modulated by rTMS, such as executive dysfunction, that are transdiagnostic across these disorders. Lastly, we describe promising approaches in the personalization and optimization of rTMS that may be applicable to both AUD and MDD. By bridging the gap between research efforts in MDD and AUD, rTMS is well positioned to be developed as a treatment for the many patients who have both conditions concurrently.
... There is also evidence that spatial representations in the parietal cortex have been reused for number cognition [169], or that a part of the spatial reorienting system is involved in social perspective taking [50]. Yet another example of neural reuse is the interaction between emotion and action control [170,171], as emotional stimuli may affect motor cortex excitability [172]. Finally, some studies indicate that the human episodic memory system emerged from a spatial orienting system within the medial temporal lobes [173]. ...
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... It is established within the literature that these types of behaviours can become highly addictive and disrupt normal activities of living [17]. There are many cognitive neuroscience studies to support this hypothesis [23][24][25]. Garofalo and colleagues suggest that individual differences in learning style and cognitive abilities (i.e., working memory capacity) play a role in the predisposition to such maladaptive implications [26]. Thus, inappropriate and maladaptive behaviours might potentially show the characteristics of addiction. ...
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Hypersexuality is related to functions of personality and emotion and is a salient symptom of bipolar I disorder especially during manic episode. However, it is uncertain whether bipolar I disorder with (BW) and without (BO) hypersexuality exhibits different cerebral activations under external emotion stimuli. In 54 healthy volunteers, 27 BW and 26 BO patients, we administered the visual oddball event-related potentials (ERPs) under external emotions of Disgust, Erotica, Fear, Happiness, Neutral, and Sadness. Participants’ concurrent states of mania, hypomania, and depression were also evaluated. The N1 latencies under Erotica and Happiness were prolonged, and the P3b amplitudes under Fear and Sadness were decreased in BW; the P3b amplitudes under Fear were increased in BO. The parietal, frontal, and occipital activations were found in BW, and the frontal and temporal activations in BO under different external emotional stimuli, respectively. Some ERP components were correlated with the concurrent affective states in three groups of participants. The primary perception under Erotica and Happiness, and voluntary attention under Fear and Sadness, were impaired in BW, while the voluntary attention under Fear was impaired in BO. Our study indicates different patterns of visual attentional deficits under different external emotions in BW and BO.
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According to a recent theory, anterior cingulate cortex is sensitive to response conflict, the coactivation of mutually incompatible responses. The present research develops this theory to provide a new account of the error-related negativity (ERN), a scalp potential observed following errors. Connectionist simulations of response conflict in an attentional task demonstrated that the ERN—its timing and sensitivity to task parameters—can be explained in terms of the conflict theory. A new experiment confirmed predictions of this theory regarding the ERN and a second scalp potential, the N2, that is proposed to reflect conflict monitoring on correct response trials. Further analysis of the simulation data indicated that errors can be detected reliably on the basis of post-error conflict. It is concluded that the ERN can be explained in terms of response conflict and that monitoring for conflict may provide a simple mechanism for detecting errors.
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We tested the hypothesis that an unconscious preattentive perceptual analysis of phobic stimuli is sufficient to elicit human fear responses. Selected snake- and spider-fearful Ss, as well as normal controls, were exposed to pictures of snakes, spiders, flowers, and mushrooms. A separate forced-choice recognition experiment established backward masking conditions that effectively precluded recognition of experimental stimuli both for fearful and nonfearful Ss. In the main experiment, these conditions were used to compare skin conductance responses (SCRs) to masked and nonmasked phobic and control pictures among fearful and nonfearful Ss. In support of the hypotheses, snake- and spider-fearful Ss showed elevated SCRs to snake and spider pictures as compared with neutral pictures and with responses of the nonfearful Ss under both masking conditions. Ratings of valence, arousal, and dominance indicated that the fearful Ss felt more negative, more aroused, and less dominant in relation to both masked and nonmasked phobic stimuli.
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The ability to rapidly process others’ emotional signals is crucial for adaptive social interactions. However, to date it is still unclear how observing emotional facial expressions affects the reactivity of the human motor cortex. To provide insights on this issue, we employed single-pulse tran-scranial magnetic stimulation (TMS) to investigate corticospinal motor excitability. Healthy par-ticipants observed happy, fearful and neutral pictures of facial expressions while receiving TMS over the left or right motor cortex at 150 and 300 ms after picture onset. In the early phase (150 ms), we observed an enhancement of corticospinal excitability for the observation of happy and fearful emotional faces compared to neutral expressions specifically in the right hemisphere. Interindi-vidual differences in the disposition to experience aversive feelings (personal distress) in inter-personal emotional contexts predicted the early increase in corticospinal excitability for emo-tional faces. No differences in corticospinal excitability were observed at the later time (300 ms) or in the left M1. These findings support the notion that emotion perception primes the body for action and highlights the role of the right hemisphere in implementing a rapid and transient fa-cilitatory response to emotional arousing stimuli, such as emotional facial expressions.
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The stop-signal paradigm, a primary experimental paradigm for understanding cognitive control and response inhibition, rests upon the theoretical foundation of race models, which assume that a go process races independently against a stop process that occurs after a stop-signal delay (SSD). We show that severe violations of this independence assumption at short SSDs occur systematically across a wide range of conditions, including fast and slow reaction times, auditory and visual stop signals, manual and saccadic responses, and especially in selective stopping. We also reanalyze existing data and show that conclusions can change when short SSDs are excluded. Last, we suggest experimental and analysis techniques to address this violation, and propose adjustments to extant models to accommodate this finding.
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Environmental cues may anticipate the availability of rewards, thus acting as a guide towards a specific choice (i.e. cue-guided choices). Despite the lateral prefrontal cortex having a critical role in using past learning and flexibly selecting relevant information to guide behavior, the literature on the neural basis of human cue-guided choice mainly focused on the subcortical brain structures implicated, while the specific role of cortical areas remained unclear. The present study aimed to provide causal evidence for the involvement of the lateral prefrontal cortex in two forms of human cue-guided choice, namely outcome-specific and general. To do this, 2 mA cathodal, anodal or sham transcranial direct current stimulation was applied over the lateral prefrontal cortex (with the posterior parietal cortex serving as control region) in three separate groups performing a Pavlovian-to-Instrumental Transfer task. Results showed, for the first time, a dissociation in the cortical structures involved in human cue-guided choice. Cathodal stimulation of the lateral prefrontal cortex reduced the outcome-specific transfer. In striking contrast, there was no influence on the general transfer. These results argue in favor of the presence of at least two possible neural pathways underlying cue-guided choices.
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The impairment of inhibitory control is often assumed to be the core deficit of several neurodevelopmental disorders characterized by poor impulse control. However, could the same deficit explain different clinical phenotypes? Evidence from behavioural studies is very mixed. This is partly because inhibition is a highly complex executive function. Thus, the different types of tasks that generically tap into inhibitory control are likely to provide different outcomes. Additionally, sample inhomogeneity in terms of age, comorbidity, and medical treatment are confounding factors. Therefore, to make a reliable assessment of the deficit of inhibitory control in a given disorder, the same task and samples with similar characteristics must be employed. This article reviews and discusses studies on five neurodevelopmental disorders with impaired impulse control where these criteria have been used: Tourette syndrome; obsessive–compulsive disorder; attention‐deficit/hyperactivity disorder; primary motor stereotypies; and autism spectrum disorder. Overall, they suggest that the mechanisms underlying the inability to control urges are extremely heterogeneous and cannot be ascribed to a general impairment of inhibition. These findings do not support the hypothesis that inhibitory deficits represent a transdiagnostic feature of neurodevelopmental disorders with poor impulse control. What this paper adds The mechanisms underlying the inability to control urges in neurodevelopmental disorders are heterogeneous. Inhibition impairments cannot generally explain all neurodevelopmental disorders characterized by poor urge control.
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Facial emotional expressions are a salient source of information for nonverbal social interactions. However, their impact on action planning and execution is highly controversial. In this vein, the effect of the two threatening facial expressions, i.e., angry and fearful faces, is still unclear. Frequently, fear and anger are used interchangeably as negative emotions. However, they convey different social signals. Unlike fear, anger indicates a direct threat toward the observer. To provide new evidence on this issue, we exploited a novel design based on two versions of a Go/No-go task. In the emotional version, healthy participants had to perform the same movement for pictures of fearful, angry, or happy faces and withhold it when neutral expressions were presented. The same pictures were shown in the control version, but participants had to move or suppress the movement, according to the actor's gender. This experimental design allows us to test task relevance's impact on emotional stimuli without conflating movement planning with target detection and task switching. We found that the emotional content of faces interferes with actions only when task-relevant, i.e., the effect of emotions is context-dependent. We also showed that angry faces qualitatively had the same effect as fearful faces, i.e., both negative emotions decreased response readiness with respect to happy expressions. However, anger has a much greater impact than fear, as it increases both the rates of mistakes and the time of movement execution. We interpreted these results, suggesting that participants have to exploit more cognitive resources to appraise threatening than positive facial expressions, and angry than fearful faces before acting.
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The role of the ventromedial prefrontal cortex (vmPFC) in human pavlovian threat conditioning has been relegated largely to the extinction or reversal of previously acquired stimulus-outcome associations. However, recent neuroimaging evidence questions this view by also showing activity in the vmPFC during threat acquisition. Here we investigate the casual role of vmPFC in the acquisition of pavlovian threat conditioning by assessing skin conductance response (SCR) and declarative memory of stimulus-outcome contingencies during a differential pavlovian threat-conditioning paradigm in eight patients with a bilateral vmPFC lesion, 10 with a lesion outside PFC and 10 healthy participants (each group included both females and males). Results showed that patients with vmPFC lesion failed to produce a conditioned SCR during threat acquisition, despite no evidence of compromised SCR to unconditioned stimulus or compromised declarative memory for stimulus-outcome contingencies. These results suggest that the vmPFC plays a causal role in the acquisition of new learning and not just in the extinction or reversal of previously acquired learning, as previously thought. Given the role of the vmPFC in schema-related processing and latent structure learning, the vmPFC may be required to construct a detailed representation of the task, which is needed to produce a sustained conditioned physiological response in anticipation of the unconditioned stimulus during threat acquisition.
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Objective: Based on the ideation-to-action framework of suicidality, this study aimed to examine whether suicide attempters differ from suicide ideators or nonsuicidal controls in response inhibition under emotional context. Method: A total of 142 community adults with lifetime history of suicide ideation or attempt as well as nonsuicidal controls were recruited. All participants completed an emotional stop-signal task and self-report measures of impulsivity. Results: In the stop-signal task, suicide attempters did not differ from ideators in response inhibition under emotional context. Moreover, both attempters and ideators did not differ from nonsuicidal controls in response inhibition to negative emotions. Compared with nonsuicidal controls, suicide ideators and attempters exhibited poorer response inhibition to positive emotions in the threat context but not in the nonthreat context. Using self-report measures, it was found that only negative urgency differentiated suicide attempters from ideators or nonsuicidal controls. Conclusions: These results suggest that people who have thought about or attempted suicide have impaired response inhibition toward positive emotional stimuli in threat contexts but not toward negative emotional stimuli. However, suicide attempters perceived themselves as more impulsive when experiencing negative emotional states as compared with suicide ideators and nonsuicidal controls.
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Response inhibition is a critical cognitive ability underlying executive control over reactions to external cues, or inner requirements. Previous studies suggest that high arousal negative emotions (e.g., anger or fear) could impair response inhibition in implicit emotional stop signal tasks (eSSTs). However, studies exploring how low arousal negative emotions (e.g., sadness) influence response inhibition remain sparse. In the current study, 20 female college students performed an explicit eSST to explore the influence of sadness on response inhibition and its neural mechanism. Participants are instructed to press a button to sad or neutral facial stimuli while inhibiting their response during the presentation of a stop signal. Results showed that compared with neutral stimuli, sad stimuli were related to increased stop signal reaction time (SSRT) (i.e., worse response inhibition). Compared with neutral condition, higher activation during sad condition was found within the right superior frontal gyrus (SFG), right insula, right middle cingulate cortex (MCC), bilateral superior temporal gyrus (STG), left lingual gyrus, and right motor cortex. These findings indicated that sadness, like other negative emotions, may impair response inhibition in an explicit way and highlight the explicit eSST as a new paradigm to investigate the subtle interaction between negative emotion processing and cognitive control.
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Emotional information is integral to everyday life and impacts a variety of cognitive abilities including response inhibition, a critical skill for maintaining appropriate and flexible behaviour. However, reported effects of emotion on response inhibition are inconsistent in younger adults, and very limited in older adults. Effects of aging are especially relevant because emotion regulation improves with aging despite declining inhibitory control over neutral information. Across three studies, we assessed the impact of emotional facial expressions on response inhibition in younger and older adults while manipulating attention to task stimuli. Emotional faces (versus neutral faces) altered response inhibition only when task instructions required explicit attention to emotional attributes of the faces. When directly comparing fear faces to happy faces, both age groups had better response inhibition to happy faces. Age further influenced differences across conditions, in that happy faces enhanced response inhibition relative to neutral faces in older adults but not younger adults. Thus, emotional response inhibition for task-relevant (but not task-irrelevant) positive information is enhanced in late life compared to early adulthood. The present work extends the nascent literature on emotional response inhibition in aging, and proffers a framework to reconcile the mixed literature on this topic in younger adults.
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Schizophrenia subjects have shown deficits of inhibition in conditions such as a stop signal task. The stop signal response time (SSRT) is consistently longer compared with healthy controls, and is accompanied by decreased brain activations in the right inferior frontal gyrus. However, as to how the response inhibition function is supported by distributed brain networks, and whether such networks are altered in schizophrenia are largely unknown. We analyzed functional MRI data of a stop signal task from 44 schizophrenia patients and 44 matched controls, and performed whole-brain psychophysiological interaction analysis to obtain task-modulated connectivity (TMC). Support vector classification was used to classify schizophrenia, and support vector regression was applied to explore the relationships between TMC and behavior indexes, such as SSRT. Schizophrenia group showed a decreased TMC pattern which mainly involved the fronto-parietal network, and increased TMC related to the sensorimotor network. Moreover, TMC could only successfully predict SSRT in the control group, further suggesting an abnormal task modulation in schizophrenia. Lastly, we compared the classification and prediction results from different types of measures, i.e., TMC, task-independent connectivity (TIC), task-functional connectivity (TFC), and resting-state functional connectivity (RSFC). TMC performed better in the behavior predictions, while TIC performed better in the classification. TFC and RSFC had similar classification and prediction performance as TIC. The current results provide new insights into the altered brain functional integration underlying response inhibition in schizophrenia, and suggest that different types of connectivity measures are complementary for a better understanding of brain networks and their alterations.
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Background: Schizophrenia (SCH) patients are at high risk for obsessive-compulsive syndrome, which can lead to difficulty in differential diagnosis between SCH and obsessive-compulsive disorder (OCD). It would be of great clinical value to identify objective markers for these diseases based on behavioral or neurological manifestations. Deficient response inhibition has been reported in both SCH and OCD; however, it is unclear if common or distinct neural abnormalities underlie this impairment. Methods: To address this question, we compared Stop signal task performance and associated event-related potentials (ERPs) and event-related oscillation (ERO) among 24 SCH patients, 25 OCD patients, and 27 healthy controls (HCs). Results: In successful Stop trials, both SCH and OCD patients showed prolonged Stop signal response time, reduced ERP-P3 component amplitude, and weaker theta-band synchronization compared to HCs, while there were no significant differences between patient groups. In unsuccessful Stop trials, however, SCH patients demonstrated significantly lower P3 amplitudes and weaker theta-band activity than OCD patients. In addition, Stop accuracy rate in SCH patients was negatively correlated with Positive subscale score of the Positive and Negative Syndrome Scale. Conclusions: These results provide evidence that impaired response inhibition in SCH and OCD arises from common underlying neural processing abnormalities. However, the lower P3 amplitude and weaker theta-band activity in SCH patients in unsuccessful Stop trials suggest distinct neural activity patterns related to error processing. These differences in ERPs and ERO may provide clues to unique neurological abnormalities in SCH and provide objective measures for differential diagnosis.
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Objective Inhibitory control is a key deficit in patients with schizophrenia. This study aims to test whether emotions can facilitate inhibition in patients with schizophrenia when they increase attention to inhibitory process. Method A total of 36 patients with schizophrenia and 36 healthy controls completed an emotional stop-signal task. The task involved selective responses to “Go” stimuli and stopped response when emotional or neutral stop cues occurred. Results In all conditions, patients with schizophrenia took longer time to inhibit response compared with healthy controls, indicating an overall impairment in response inhibition. Importantly, patients with schizophrenia and controls acquired similar size of benefit from the negative stop cues, showing as reduced reaction time to negative than neutral stop cues. However, the negative stop cues impaired subsequent Go performance only in patients with schizophrenia, indicating additional cost of the negative stop cues for patients with schizophrenia. In both groups, the positive stop cues did not have any significant influence on response inhibition. Conclusions These findings provide novel evidence for the benefit of emotional stop cues on inhibitory control in patients with schizophrenia and reveal different after-effects of emotional enhancement effect in patients and healthy populations. The findings may help develop effective interventions for improving inhibitory control in patients with schizophrenia and other clinical populations.
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