Introduction Cognitive dysfunction and emotional symptoms frequently co-occur in Parkinson’s disease (PD), yet the processes linking these domains remain unclear. One proposed pathway involves differences in emotion regulation (ER) strategy use, which may vary as a function of cognitive functioning. Methods This study examined whether task-based executive functioning (EF) and self-reported functional cognitive impairment (FCI) are associated with anxiety, depression, and mental wellbeing in PD, and whether these relationships are moderated by ER strategies. One hundred and three individuals with PD completed EF tasks, and self-report measures of FCI, ER strategy use, and mental health. Principal component analysis was used to derive task-based EF components. Moderation analyses tested whether self-reported and task-based cognitive functioning interacted with ER strategy use in relation to mental health outcomes. Results Greater FCI was associated with stronger negative relationships between Seeking Distractions and Ignoring and mental wellbeing, and with higher anxiety and depression when Ignoring was used. Among those with better functional cognition, Withdrawal and Catastrophizing were more strongly related to poorer mental wellbeing, while Putting into Perspective was associated with lower depressive symptoms. Stronger task-based Executive and Inhibitory Control were associated with weaker relationships between Ignoring and anxiety and depression, respectively, whereas greater Acceptance was associated with higher anxiety among those with stronger Executive Control. Conclusions Cognitive functioning moderates the relationship between ER strategies and mental health outcomes in PD. Functional cognition showed more consistent associations, whereas task-based EF exerted more limited effects. These findings contribute to understanding variability in affective symptoms in PD.

Reduced heart rate variability (HRV) at rest has been associated with negative emotions not only in adults but also in adolescents. Given that poverty can be a significant source of stress and negative emotional states, family socioeconomic backgrounds may be associated with adolescents' HRV, negative mood, as well as perceived stress. However, the currently available evidence heavily relies on findings based on the so-called "Minority World," including western and developed countries. To address the significance of HRV and socioeconomic status in adolescents in the Majority world, in the present study, we assessed resting-state HRV, socioeconomic status, and depression in adolescents from Nigeria. We also assessed their mood and perceived stress for four consecutive days. The results indicated that socioeconomic backgrounds were not significantly associated with self-report measures on mood, perceived stress, and depression. However, we found that lower levels of socioeconomic background are associated with lower levels of resting-state HRV. These results suggest that HRV is sensitive to poverty-related stress in previously under-investigated samples-adolescents in Nigeria.

Cognitive reappraisal is a fundamental emotion regulation strategy for mental and physical well-being, but how its neural mechanisms relate to individual differences remains poorly understood. In a consortium effort analyzing 40 fMRI datasets ( N =2,175), we examined the relationship between neural activation during reappraisal tasks and three core individual difference indices of reappraisal capabilities: (1) trait questionnaires, (2) task-based affective ratings, and (3) amygdala down-regulation. Strikingly, there was no shared overlap across these three common indices. Only a very weak correlation emerged between amygdala down-regulation and task-based affective ratings. Whole-brain analyses revealed no reliable neural associations with trait questionnaires, and associations with task-based affective ratings fell outside canonical emotion regulation networks (e.g., prefrontal circuitry). Moreover, amygdala down-regulation, often interpreted as a stable individual marker, was confounded by person-specific whole-brain responses — a limitation extending to fMRI research beyond the emotion regulation domain. These findings challenge the assumption that an individual’s prefrontal activity is a valid indicator of their reappraisal capabilities and suggest that common trait, behavioral, and neural measures might capture distinct facets of emotion regulation. More broadly, our results highlight concrete methodological challenges for fMRI research on individual differences, with implications extending beyond emotion regulation to the neuroscience of personality, psychopathology, and general well-being. ### Competing Interest Statement The authors have declared no competing interest.

Background: Cognitive dysfunction and emotional symptoms frequently co-occur in Parkinson’s disease (PD), yet the mechanisms linking these domains have yet to be clearly defined. One proposed pathway involves differences in emotion regulation (ER) strategy use, which may vary as a function of cognitive capacity.Objectives: To examine whether task-based executive functioning (EF) and self-reported functional cognitive impairment (FCI) are associated with anxiety, depression, and mental wellbeing in PD, and whether these relationships are mediated or moderated by ER strategies.Methods: 103 individuals with PD completed EF tasks, as well as self-report measures of FCI, ER strategy use, and mental health. Principal component analysis was used to derive EF components. Mediation and moderation analyses examined whether cognitive functioning predicted mental health through or in interaction with ER strategy use.Results: Worse FCI was directly associated with poorer mental health and linked to greater use of maladaptive strategies. Better task-based EF was indirectly associated with better mental health outcomes via increased use of adaptive ER strategies. The association between regulation strategies and mental health varied depending on cognitive capacity, suggesting that the effectiveness of specific strategies is contingent on underlying cognitive functioning.Conclusions: These findings identify cognitive capacity as a key underpinning of ER and its relationship to mental health outcomes in PD. By delineating distinct contributions of functional and task-based cognition, this study advances understanding of the mechanisms underlying affective symptom expression in PD and highlights the cognitive context in which non-motor symptoms emerge.

Meta-analyses of functional magnetic resonance imaging (fMRI) studies have identified networks of widely distributed brain regions supporting emotion regulation. These overlap with attentional or cognitive control brain networks. The literature is short on data speaking to specific neurocognitive functions of these broad brain networks in reappraisal - a key emotion regulatory strategy involving the reframing of an event according to a goal to increase or decrease experienced emotion. We address this gap by examining both the spatial configuration and temporal profile of event-related blood oxygenation level dependent (BOLD) responses during a task requiring reappraisal. We analysed fMRI datasets obtained from 84 participants (51% female) who were instructed to increase or decrease their emotional response to unpleasant images. We extracted spatial maps and their estimated temporal event-related BOLD signal changes of four components with the highest loadings. Neurocognitive functions were derived by mapping each component onto templates of previously identified task-based cognitive modes. This analysis yielded four cognitive modes: 1) “multiple demand” 2) “response”, 3) “re-evaluation”, and 4) “default mode". The temporal profiles showed particularly prominent patterns for the increase and decrease conditions in “multiple demand” (mode 1) and “re-evaluation” (mode 3) respectively. These findings highlight a central role for specific neurocognitive processes linked to attentional control (“multiple demand”) and switching (“re-evaluation”), as part of the broad brain networks supporting reappraisal. Moreover, the level of neural engagement of these cognitive modes varies depending on the regulatory goal. These findings provide tangible targets for neurocognitive interventions such as neurostimulation when emotion regulation is compromised. ### Competing Interest Statement The authors have declared no competing interest. Biotechnology and Biological Sciences Research Council, https://ror.org/00cwqg982, BB/J009539/1, BB/L02697X/1

Acute pain serves to warn an organism of potential damage. Two plausible theoretical response scenarios for prolonged painful stimulation could be hypothesised: If the organism does not sense potential harm an individual may habituate. Whereas, if harm is possible, pain sensitization may be more probable. Examining how an individual adapts to prolonged stimulation will provide unique insight into the mechanisms underlying pain habituation and sensitisation and, potentially, a valuable perspective on the development of chronic pain. However, currently little is known about the stability of these individual differences or their underlying neural mechanisms. To address this, 85 participants completed an MRI session, involving a noxious stimulation task and a resting-state scan. Habituation/sensitization was operationalized as the slope of change in pain ratings across the task. Habituation was associated with increasing activity in the anterior hippocampus and amygdala over time, with sensitization associated with increasing activity in the sensorimotor cortices. These regions were then used as seeds for a resting-state functional connectivity analysis, which revealed that habituation was associated with higher connectivity between the hippocampus and ventromedial prefrontal cortex, as well as higher connectivity between sensorimotor regions and the hippocampus, amygdala, and insula cortex. We have shown that habituation/sensitization to pain is a stable trait underpinned by differential activity in brain regions supporting sensory processing and appraisal. The perspective of these stable phenotypical patterns could have clinical applications and potential for improving our understanding of the development of chronic pain.

Pavlovian fear conditioning is a fundamental process in both health and disease. We investigate its neural correlates and sources of variability using harmonized functional magnetic resonance imaging data from 2199 individuals across nine countries, including 1888 healthy individuals and 311 with anxiety-related or depressive disorders. Using mega-analysis and normative modeling, we show that fear conditioning consistently engages brain regions within the "central autonomic-interoceptive" or "salience" network. Several task variables strongly modulate activity in these regions, contributing to variability in neural responses. Additionally, brain activation patterns differ between healthy individuals and those with anxiety-related or depressive disorders, with distinct profiles characterizing specific disorders such as post-traumatic stress disorder and obsessive-compulsive disorder. While the neural correlates of fear conditioning are highly generalizable at the population level, variability arises from differences in task design and clinical status, highlighting the importance of methodological diversity in capturing fear learning mechanisms.

Understanding and sharing others' emotions (i.e., empathy) requires the ability to manage one's own emotions (i.e., emotion regulation). Indeed, empirical evidence suggests that empathy and emotion regulation are related. This evidence is largely based on self-report measures of both constructs. The current study examined how task measures that assess processes related to empathy are associated with self-reported emotion dysregulation in a young adult sample. An eye-tracking-based perspective-taking task was used as a proxy measure of cognitive empathy. A spontaneous facial mimicry (SFM) task, wherein the activation of the Zygomaticus Major and the Corrugator Supercilii was measured during the passive viewing of happy and angry faces, was used as a proxy measure of affective empathy. The perspective-taking task metric showed a negative relationship with emotion dysregulation. The overall SFM metric was not significantly associated with emotion dysregulation. Follow-up analyses revealed that SFM for angry faces was inversely proportional to emotion dysregulation; no such relationship was observed for SFM for happy faces. These findings build upon prior work by demonstrating a positive relationship between adaptive emotion regulation and a behavioral measure of cognitive empathy. The findings for affective empathy are suggestive of a valence-specific relationship between SFM and emotion regulation.

OBJECTIVE:Recent theoretical work suggests that the expression of emotions may differ among Black and White Americans, such that Black Americans engage more frequently in expressive suppression to regulate emotions and avoid conflict. Prior work has linked expressive suppression usage with increases in cardiovascular disease risk, suggesting that racialized differences in expressive suppression usage may be one mechanism by which racism "gets under the skin" and creates health disparities. METHOD:To examine racialized differences in expressive suppression and blood pressure (a measure of cardiovascular disease risk), we used self-report and facial electromyography (fEMG) data from two cohorts of Black and White Americans from the Midlife in the United States (MIDUS) longitudinal study (MIDUS 2, n = 271, 34.7% Black, collected from 2004 to 2009; MIDUS Refresher 1, n = 114, 31.6% Black, collected from 2012 to 2016; total N = 385, 33.9% Black). RESULTS:Black Americans reported engaging in expressive suppression more frequently than White Americans ( t (260.95) = 2.18, p = .002) and showed less corrugator fEMG activity during negative images ( t (969) = 2.38, pFDR = .026). Less corrugator activity during negative images was associated with higher systolic blood pressure only for Black Americans ( b = -4.63, t (375) = 2.67, p = .008). CONCLUSION:Overall, results are consistent with theoretical accounts that Black Americans engage more frequently in expressive suppression, which in turn is related to higher cardiovascular risk. Additional research is needed to further test this claim, particularly in real-world contexts and self-reports of in-the-moment usage of expressive suppression.

The ratio of fronto‐central theta (4–7 Hz) to beta oscillations (13–30 Hz), known as the theta-beta ratio, is negatively correlated with attentional control, reinforcement learning, executive function, and age. Although theta-beta ratios have been found to decrease with age in adolescents and young adults, theta has been found to increase with age in older adults. Moreover, age‐related decreases in individual alpha peak frequency and flattening of the 1/f aperiodic component may artifactually inflate the association between theta-beta ratio and age. These factors lead to an incomplete understanding of how theta-beta ratio varies across the lifespan and the extent to which variation is due to a conflation of aperiodic and periodic activity. We conducted a partially preregistered analysis examining the cross‐sectional associations between age and resting canonical fronto-central theta-beta ratio, individual alpha peak frequency, and aperiodic component (n = 268; age 36–84, M = 55.8, SD = 11.0). Age was negatively associated with theta-beta ratios, individual peak alpha frequencies, and the aperiodic exponent. The correlation between theta-beta ratios and age remained after controlling for individual peak alpha frequencies, but was non-significant when controlling for the aperiodic exponent. Aperiodic exponent fully mediated the relationship between theta-beta ratio and age, although beta remained significantly associated with age after controlling for theta, individual peak alpha, and aperiodic exponent. Results replicate previous observations and show age‐related decreases in theta-beta ratios are not due to age‐related decreases in individual peak alpha frequencies but primarily explained by flattening of the aperiodic component with age.

Curiosity-the intrinsic desire to know-is a concept central to thehuman mind and knowledge acquisition. Experimental studies oninformation-seeking have found that curiosity facilitates memory encoding andexhibits similar rewarding properties as extrinsic rewards/incentives, byeliciting a dopaminergic response in the reward network. However, it is notclear whether these findings hold with more naturalistic dynamic stimuli and howthe joint effect of curiosity and extrinsic incentive manifests in learning andneural activation patterns. Herein, we presented participants with videos ofmagic tricks across two behavioural (N1= 77, N2= 78) and one fMRI study (N = 50) and asked them to ratesubjective feelings of curiosity, while also performing a judgement task thatwas incentivised for the half of participants. Incidental memory for the magictrick was tested a week later. The integrated results showed that both curiosityand availability of extrinsic incentives enhanced encoding but did not interactwith each other. However, curiosity influenced only high-confidence recognitionmemory, whereas extrinsic incentives affected memory regardless of confidence,suggesting the involvement of different encoding mechanisms. Analysis of thefMRI data using the intersubject synchronisation framework showed that, whilethe effects of curiosity on memory were located in the hippocampus anddopaminergic brain areas, neither the effects of curiosity nor incentivesthemselves were found in the often-implicated reward network. Instead, they wereassociated with cortical areas involved in processing uncertainly and attention.These results challenge a traditional focus on reward networks in curiosity andhighlight the involvement of broader brain networks.

The aim of the present study was to examine the acute and chronic effects of wild blueberry supplementation on mood, executive function, and serum biomarkers of neuroplasticity, inflammation, and oxidative stress in emerging adults with moderate-to-severe depressive symptoms. In this double-blind trial, 60 emerging adults (Mage = 20.0 years, 32

Although exposure-based therapy has been found to be effective at alleviating symptoms of social anxiety disorder, it often does not lead to full remission, and relapse after treatment is common. Exposure therapy is based on theoretical principles of extinction of conditioned fear responses. However, there are inconsistencies in findings across experiments that have investigated the effect of social anxiety on threat conditioning and extinction processes. This systematic review and meta-analysis aimed to examine whether elevated levels of social anxiety are associated with abnormalities in threat conditioning and extinction processes. A second aim was to examine the sensitivity of various study designs and characteristics to detect social anxiety-related differences in threat conditioning and extinction. A systematic search was conducted, which identified twenty-three experiments for inclusion in the review. The findings did not demonstrate compelling evidence that high levels of social anxiety are associated with atypical threat conditioning or extinction. Further, when systematically examining the data, there was no convincing support that the use of a particular psychophysiological measure, subjective rating, or experimental parameter yields more consistent associations between social anxiety and conditioning processes during threat acquisition or extinction. Meta-analyses demonstrated that during threat extinction, the use of anxiety ratings as a dependent variable, socially relevant unconditioned stimuli, and a higher reinforcement schedule produced more detectable effects of social anxiety on compromised extinction processes compared to any other dependent variable (subjective or physiological) or experimental parameter. Overall, the results of this study suggest that social anxiety is not reliably related to deficits in conditioning and extinction processes in the context of laboratory-based Pavlovian conditioning paradigms.

Measures of intrinsic brain function at rest show promise as predictors of cognitive decline in humans, including EEG metrics such as individual alpha peak frequency (IAPF) and the aperiodic exponent, reflecting the strongest frequency of alpha oscillations and the relative balance of excitatory/inhibitory neural activity, respectively. Both IAPF and the aperiodic exponent decrease with age and have been associated with worse executive function and working memory. However, few studies have jointly examined their associations with cognitive function, and none have examined their association with longitudinal cognitive decline rather than cross-sectional impairment. In a preregistered secondary analysis of data from the longitudinal Midlife in the United States (MIDUS) study, we tested whether IAPF and aperiodic exponent measured at rest predict cognitive function (N = 235; age at EEG recording M = 55.10, SD =10.71) over 10 years. The IAPF and the aperiodic exponent interacted to predict decline in overall cognitive ability, even after controlling for age, sex, education, and lag between data collection time points. Post hoc tests showed that "mismatched" IAPF and aperiodic exponents (e.g., higher exponent with lower IAPF) predicted greater cognitive decline compared to "matching" IAPF and aperiodic exponents (e.g., higher exponent with higher IAPF; lower IAPF with lower aperiodic exponent). These effects were largely driven by measures of executive function. Our findings provide the first evidence that IAPF and the aperiodic exponent are joint predictors of cognitive decline from midlife into old age and thus may offer a useful clinical tool for predicting cognitive risk in aging.

Introduction: Central sensitization (CS) was first defined in animal studies to be increased nociceptive responsiveness due to sensitization of neurons in the central nervous system, usually the result of prolonged nociceptive input or a disease state. Recently, the concept of CS has been adopted in clinical assessments of chronic pain, but its diagnosis in humans has expanded to include the enhancement of a wide range of nociceptive, sensory, and emotional responses. Many poorly understood pain disorders are referred to as "central sensitivity syndrome," a term associated with a broad range of hypervigilant sensory and emotional responses. Diagnosis often involves a review of medical records and an assessment of behaviour, emotional disposition, and overall sensitivity of a patient. Obviously, these assessments are unable to directly capture the responsiveness of nociceptive neurons. The purpose of this review is to ascertain whether self-report questionnaires associated with central sensitization and the diagnosis of central sensitivity syndrome are associated with enhanced nociceptive responses or whether they more validly measure sensitivity in a broader sense (ie, including emotional responses). Methods: Following the PRISMA guidelines, a detailed search of studies that involve the Central Sensitization Inventory or Pain Sensitivity Questionnaire correlated with either nociceptive sensory tests (quantitative sensory testing) or emotional hypervigilance (anxiety, depression, stress, etc) will be conducted on MEDLINE, PsychINFO, and Web of Science. Perspective: The review is expected to synthesize correlations between sensitivity questionnaires and nociceptive or emotional sensitivity to determine whether these questionnaires reflect a broadened understanding of the term "central sensitization."

Acute pain serves to warn an organism of potential damage. When nociceptive stimulation persists, two possible responses emerge: If no risk of harm is anticipated, habituation may occur. If harm is considered possible, pain sensitization is likely. An individual’s adaptation to prolonged pain may provide insight into their ability to manage resources, and possibly their likelihood of developing chronic pain. Yet, little is known about the stability of these individual differences or their underlying neural mechanisms. Eighty-five participants undertook a repetitive noxious stimulation task and a resting-state scan in an MRI scanner, in a first session. They then completed the same task outside the scanner on three separate days. Pain adaptation was operationalized as the slope of change in pain ratings within session. Intraclass correlations were calculated between slopes across the four sessions, which demonstrated high stability and association with emotional disposition. Individuals who habituated to repeated stimuli showed increasing activity in the anterior hippocampus and amygdala, while individuals who sensitized showed increasing activity in the sensorimotor cortices. These clusters were then used as seeds in resting state analysis, with habituation associated with higher functional connectivity between hippocampus/amygdala and ventromedial prefrontal cortex(vmPFC), and higher connectivity between sensorimotor regions and the hippocampus, amygdala and insula cortex. Our findings suggest that pain adaptation is a stable phenotypic trait, which may have implications for the prediction of chronic pain. This study implicates neural sensory and appraisal systems in these stable responses, offering insight into the mechanisms underlying trait-like responses to prolonged nociceptive input.

Fear conditioning is a widely used laboratory model to investigate learning, memory, and psychopathology across species. The quantification of learning in this paradigm is heterogeneous in humans and psychometric properties of different quantification methods can be difficult to establish. To overcome this obstacle, calibration is a standard metrological procedure in which well-defined values of a latent variable are generated in an established experimental paradigm. These intended values then serve as validity criterion to rank methods. Here, we develop a calibration protocol for human fear conditioning. Based on a literature review, series of workshops, and survey of N = 96 experts, we propose a calibration experiment and settings for 25 design variables to calibrate the measurement of fear conditioning. Design variables were chosen to be as theory-free as possible and allow wide applicability in different experimental contexts. Besides establishing a specific calibration procedure, the general calibration process we outline may serve as a blueprint for calibration efforts in other subfields of behavioral neuroscience that need measurement refinement.

Previous research has demonstrated that individuals with high levels of Intolerance of Uncertainty (IU) have difficulty updating threat associations to safety associations. Notably, prior research has focused on measuring IU-related differences in threat and safety learning using arousal-based measures such as skin conductance response. Here we assessed whether IU-related differences in threat and safety learning could be captured using eye-tracking metrics linked with gaze behaviours such as dwelling and scanning. Participants (N = 144) completed self-report questionnaires assessing levels of IU and trait anxiety. Eye movements were then recorded during each conditioning phase: acquisition, extinction learning, and extinction retention. Fixation count and fixation duration served as indices of conditioned responding. Patterns of threat and safety learning typically reported for physiology and self-report were observed for the fixation count and fixation duration metrics during acquisition and to some extent in extinction learning, but not for extinction retention. There was little evidence for specific associations between IU and disrupted safety learning (e.g., greater differential responses to the threat vs. safe cues during extinction learning and retention). While there was tentative evidence that IU was associated with shorter fixation durations (e.g., scanning) to threat vs. safe cues during extinction retention, this effect did not remain after controlling for trait anxiety. IU and trait anxiety similarly predicted greater fixation count and shorter fixation durations overall during extinction learning, and greater fixation count overall during extinction retention. IU further predicted shorter fixation durations overall during extinction retention. However, the only IU-based effect that remained significant after controlling for trait anxiety was that of fixation duration overall during threat extinction learning. Our results inform models of anxiety, particularly in relation to how individual differences modulate gaze behaviour during threat conditioning.

The Neurovisceral Integration Model posits that shared neural networks support the effective regulation of emotions and heart rate, with heart rate variability (HRV) serving as an objective, peripheral index of prefrontal inhibitory control. Prior neuroimaging studies have predominantly examined both HRV and associated neural functional connectivity at rest, as opposed to contexts that require active emotion regulation. The present study sought to extend upon previous resting-state functional connectivity findings, examining task-related HRV and corresponding amygdala functional connectivity during a cognitive reappraisal task. Seventy adults (52 older and 18 younger adults, 18-84 years, 51% male) received instructions to cognitively reappraise negative affective images during functional MRI scanning. HRV measures were derived from a finger pulse signal throughout the scan. During the task, younger adults exhibited a significant inverse association between HRV and amygdala-medial prefrontal cortex (mPFC) functional connectivity, in which higher task-related HRV was correlated with weaker amygdala-mPFC coupling, whereas older adults displayed a slight positive, albeit non-significant correlation. Furthermore, voxelwise whole-brain functional connectivity analyses showed that higher task-based HRV was linked to weaker right amygdala-posterior cingulate cortex connectivity across older and younger adults, and in older adults, higher task-related HRV correlated positively with stronger right amygdala-right ventrolateral prefrontal cortex connectivity. Collectively, these findings highlight the importance of assessing HRV and neural functional connectivity during active regulatory contexts to further identify neural concomitants of HRV and adaptive emotion regulation.