Whole-brain mapping of increased manganese levels in welders and its association with exposure and motor function.

Although manganese (Mn) is a trace metal essential for humans, chronic exposure to Mn can cause accumulation of this metal ion in the brain leading to an increased risk of neurological and neurobehavioral health effects. This is a concern for welders exposed to Mn through welding fumes. While brain Mn accumulation in occupational settings has mostly been reported in the basal ganglia, several imaging studies also revealed elevated Mn in other brain areas. Since Mn functions as a magnetic resonance imaging (MRI) T1 contrast agent, we developed a whole-brain MRI approach to map in vivo Mn deposition differences in the brains of non-exposed factory controls and exposed welders. This is a cross-sectional analysis of 23 non-exposed factory controls and 36 exposed full-time welders from the same truck manufacturer. We collected high-resolution 3D MRIs of brain anatomy and R1 relaxation maps to identify regional differences using voxel-based quantification (VBQ) and statistical parametric mapping. Furthermore, we investigated the associations between excess Mn deposition and neuropsychological and motor test performance. Our results indicate that: (1) Using whole-brain MRI relaxometry methods we can generate excess Mn deposition maps in vivo, (2) excess Mn accumulation due to occupational exposure occurs beyond the basal ganglia in cortical areas associated with motor and cognitive functions, (3) Mn likely diffuses along white matter tracts in the brain, and (4) Mn deposition in specific brain regions is associated with exposure (cerebellum and frontal cortex) and motor metrics (cerebellum and hippocampus).

Distinct profiles of anhedonia and reward processing and their prospective associations with quality of life among individuals with mood disorders.

Leading professional health bodies have called for the wider adoption of Patient Reported Outcome Measures, such as quality of life, in research and clinical practice as a means for understanding why the global burden of depression continues to climb despite increased rates of treatment use. Here, we examined whether anhedonia-an often recalcitrant and impairing symptom of depression-along with its neural correlates, was associated with longitudinal changes in patient-reported quality of life among individuals seeking treatment for mood disorders. We recruited 112 participants, including n = 80 individuals with mood disorders (58 unipolar, 22 bipolar) and n = 32 healthy controls (63.4% female). We assessed anhedonia severity along with two electroencephalographic markers of neural reward responsiveness (scalp-level 'Reward Positivity' amplitude and source-localized reward-related activation in the dorsal anterior cingulate cortex), and assessed quality of life at baseline, 3- and 6-month follow-up. Anhedonia emerged as a robust correlate of quality of life cross-sectionally and longitudinally among individuals with mood disorders. Furthermore, increased neural reward responsiveness at baseline was associated with greater improvements in quality of life over time, and this improvement was mediated by longitudinal improvements in anhedonia severity. Finally, differences in quality of life observed between individuals with unipolar and bipolar mood disorders were mediated by differences in anhedonia severity. Our findings indicate that anhedonia and its reward-related neural correlates are linked to variability in quality of life over time in individuals with mood disorders. Treatments capable of improving anhedonia and normalizing brain reward function may be necessary for improving broader health outcomes for individuals seeking treatment for depression.ClinicalTrials.gov identifier: NCT01976975.

Mismatch negativity and clinical trajectories in psychotic disorders: Five-year stability and predictive utility.

BACKGROUND: Mismatch negativity (MMN) amplitude is reduced in psychotic disorders and associated with symptoms and functioning. Due to these robust associations, it is often considered a biomarker for psychotic illness. The relationship between MMN and clinical outcomes has been examined well in early onset psychotic illness; however, its stability and predictive utility in chronic samples are not clear. METHOD: We examined the five-year stability of MMN amplitude over two timepoints in individuals with established psychotic disorders (cases; N = 132) and never-psychotic participants (NP; N = 170), as well as longitudinal associations with clinical symptoms and functioning. RESULTS: MMN amplitude exhibited good temporal stability (cases, r = 0.53; never-psychotic, r = 0.52). In cases, structural equation models revealed MMN amplitude to be a significant predictor of worsening auditory hallucinations (ß = 0.19), everyday functioning (ß = -0.13), and illness severity (ß = -0.12) at follow-up. Meanwhile, initial IQ (ß = -0.24), negative symptoms (ß = 0.23), and illness severity (ß = -0.16) were significant predictors of worsening MMN amplitude five years later. CONCLUSIONS: These results imply that MMN measures a neural deficit that is reasonably stable up to five years. Results support disordered cognition and negative symptoms as preceding reduced MMN, which then may operate as a mechanism driving reductions in everyday functioning and the worsening of auditory hallucinations in chronic psychotic disorders. This pattern may inform models of illness course, clarifying the relationships amongst biological mechanisms of predictive processing and clinical deficits in chronic psychosis and allowing us to better understand the mechanisms driving such impairments over time.

Temporal dynamics of emotional processing: Parsing trial-wise variance of the late positive potential using Generalizability Theory.

The reliability of individual trial event-related potential (ERP) components extracted from electroencephalogram has been consistently questioned since ERP research began. This ambivalence is based on misunderstood assumptions stemming from Cronbach and Classical Test Theory. Contemporary methods allow for the reliability of individual ERP trials to be estimated and for analyses of these trial-level ERP components to be meaningfully parsed. We illustrate the use of Generalizability Theory procedures in estimating the reliability of trial-level ERPs using the late positive potential (LPP), a neural measure of motivated attention toward emotionally evocative stimuli. Individuals (N = 88) completed a passive viewing task while continuous EEG was recorded. Variability in trial-level LPP responses was decomposed into facets corresponding to individual differences, chronological trial within block, stimulus type, their two-way interactions, and specific stimuli. We estimated various reliability coefficients and found that both overall and category-specific person-level LPP estimates have good-to-excellent reliability, while the reliability of within-person differences (i.e., change) between arousal categories was fair for the early LPP. These results were generally consistent across time windows, but were highest early in the LPP time course. We argue that investigating reliability using trial-level data allows researchers to pursue hypotheses focused on neurophysiological dynamics that unfold over the course of an experiment and not risk false inferences (i.e., ecological fallacy) when using person-level aggregates to deduce such processes. Moreover, such analyses provide information that allows researchers to optimize their protocols by potentially reducing the number of individual trials, burden on participants, and cost, while retaining sufficient reliability.

A randomized trial of aerobic exercise for major depression: examining neural indicators of reward and cognitive control as predictors and treatment targets.

BACKGROUND: Aerobic exercise has demonstrated antidepressant efficacy among adults with major depression. There is a poor understanding of the neural mechanisms associated with these effects. Deficits in reward processing and cognitive control may be two candidate targets and predictors of treatment outcome to exercise in depression. METHODS: Sixty-six young adults aged 20.23 years (s.d. = 2.39) with major depression were randomized to 8 weeks of moderate-intensity aerobic exercise (n = 35) or light stretching (n = 31). Depressive symptoms were assessed across the intervention to track symptom reduction. Reward processing [reward positivity (RewP)] and cognitive control [error-related negativity (ERN)] were assessed before and after the intervention using event-related brain potentials. RESULTS: Compared to stretching, aerobic exercise resulted in greater symptom reduction (gs = 0.66). Aerobic exercise had no impact on the RewP (gav = 0.08) or ERN (gav = 0.21). In the aerobic exercise group, individuals with a larger pre-treatment RewP [odds ratio (OR) = 1.45] and increased baseline depressive symptom severity (OR = 1.18) were more likely to respond to an aerobic exercise program. Pre-treatment ERN did not predict response (OR = 0.74). CONCLUSIONS: Aerobic exercise is effective in alleviating depressive symptoms in adults with major depression, particularly for those with increased depressive symptom severity and a larger RewP at baseline. Although aerobic exercise did not modify the RewP or ERN, there is preliminary support for the utility of the RewP in predicting who is most likely to respond to exercise as a treatment for depression.

Electroencephalogram aperiodic power spectral slope can be reliably measured and predicts ADHD risk in early development.

The aperiodic exponent of the electroencephalogram (EEG) power spectrum has received growing attention as a physiological marker of neurodevelopmental psychopathology, including attention-deficit/hyperactivity disorder (ADHD). However, its use as a marker of ADHD risk across development, and particularly in very young children, is limited by unknown reliability, difficulty in aligning canonical band-based measures across development periods, and unclear effects of treatment in later development. Here, we investigate the internal consistency of the aperiodic EEG power spectrum slope and its association with ADHD risk in both infants (n = 69, 1-month-old) and adolescents (n = 262, ages 11-17 years). Results confirm good to excellent internal consistency in infancy and adolescence. In infancy, a larger aperiodic exponent was associated with greater family history of ADHD. In contrast, in adolescence, ADHD diagnosis was associated with a smaller aperiodic exponent, but only in children with ADHD who had not received stimulant medication treatment. Results suggest that disruptions in cortical development associated with ADHD risk may be detectable shortly after birth via this approach. Together, findings imply a dynamic developmental shift in which the developmentally normative flattening of the EEG power spectrum is exaggerated in ADHD, potentially reflecting imbalances in cortical excitation and inhibition that could contribute to long-lasting differences in brain connectivity.

Authors' reply to the commentary on "Establishing norms for error-related brain activity during the arrow Flanker task among young adults".

In their commentary on our article, "Establishing norms for error-related brain activity during the arrow Flanker task among young adults" (Imburgio et al., 2020), Clayson and colleagues (2021) voiced their concerns about our development of norms for an event-related potential measure of error monitoring, the error-related negativity (ERN). The central flaw in their commentary is the idea that because we don't know all the factors that can affect the ERN, it should not be normed. We respond to this idea, while also reiterating points made in our original manuscript: a) at present, the reported norms are not intended to be used for individual clinical assessment and b) our norms should be considered specific to the procedures (i.e., recording and processing parameters) and task used (i.e., arrow Flanker). Contrary to Clayson and colleagues' claims, we believe that information about the distribution of the ERN (i.e., our norms) in a large sample representative of those used in much of the ERN literature (i.e., unselected young adults) will be useful to the field and that this information stands to increase, not decrease, understanding of the ERN.

Pathways from performance monitoring to negative symptoms and functional outcomes in psychotic disorders.

BACKGROUND: Performance monitoring entails rapid error detection to maintain task performance. Impaired performance monitoring is a candidate pathophysiological process in psychotic disorders, which may explain the broader deficit in executive function and its known associations with negative symptoms and poor functioning. The current study models cross-sectional pathways bridging neurophysiological measures of performance monitoring with executive function, symptoms, and functioning. METHODS: Data were from the 20-year assessment of the Suffolk County Mental Health Project. Individuals with psychotic disorders (N = 181) were originally recruited from inpatient psychiatric facilities. Data were also collected from a geographically and demographically matched group with no psychosis history (N = 242). Neural measures were the error-related negativity (ERN) and error positivity (Pe). Structural equation modeling tested mediation pathways. RESULTS: Blunted ERN and Pe in the clinical cohort related to impaired executive function (r = 0.26-0.35), negative symptom severity (r = 0.17-0.25), and poor real-world functioning (r = 0.17-0.19). Associations with executive function were consistent across groups. Multiple potential pathways were identified in the clinical cohort: reduced ERN to inexpressivity was mediated by executive function (ß = 0.10); reduced Pe to global functioning was mediated by executive function and avolition (ß = 0.10). CONCLUSIONS: This supports a transdiagnostic model of psychotic disorders by which poor performance monitoring contributes to impaired executive function, which contributes to negative symptoms and poor real-world functioning. If supported by future longitudinal research, these pathways could inform the development of targeted interventions to address cognitive and functional deficits that are central to psychotic disorders.

Mother-infant convergence of event-related potentials elicited by face and object processing.

Prior work has provided conceptual support for developmental changes in face and object processing, such that: face processing, as captured by the N290 event-related potential (ERP) component in infancy, may develop into the N170 in adulthood; and motivated attention, as captured by the negative central (Nc) in infancy, may develop into the late positive potential (LPP). The present study examined these neural correlates in 12-month-old infants and their mothers (N = 33 dyads). Dyads completed a viewing task consisting of familiar and novel face and toy stimuli while electroencephalography was recorded. Results suggest that for mothers, the N170 was larger for faces than toys, regardless of familiarity, and the LPP was largest for familiar faces. In infants, the N290 was somewhat larger for faces than toys (p < .10); the Nc did not vary by condition. Adult ERPs demonstrated fair to good reliability; reliability of infant ERPs was lower and was influenced by looking behaviors. Intergenerational associations were strongest between the LPP and Nc, particularly when electrode and time window were taken into account. Refinement of data handling and ERP scoring procedures for infant ERPs are crucial next steps for estimation of intergenerational associations and further examination of developmental changes in face and object processing.

Establishing norms for error-related brain activity during the arrow Flanker task among young adults.

Psychological assessments typically rely on self-report and behavioral measures. Augmenting these with neurophysiological measures of the construct in question may increase the accuracy and predictive power of these assessments. Moreover, thinking about neurophysiological measures from an assessment perspective may facilitate under-utilized research approaches (e.g., brain-based recruitment of participants). However, the lack of normative data for most neurophysiological measures has prevented the comparison of individual responses to the general population, precluding these approaches. The current work examines the distributions of two event-related potentials (ERPs) commonly used in individual differences research: the error-related negativity (ERN) and error positivity (Pe). Across three lab sites, 800 unselected participants between the ages of 18 and 30 performed the arrow version of a Flanker task while EEG was recorded. Percentile scores and distributions for ERPs on error trials, correct trials, and the difference (ΔERN, ΔPe; error minus correct) at Fz, Cz and Pz are reported. The 25th, 50th, and 75th percentile values for the ΔERN at Cz were -2.37 â€‹µV, -5.41 â€‹µV, and -8.65 â€‹µV, respectively. The same values for ΔPe at Cz were 7.51 â€‹µV, 11.18 â€‹µV, and 15.55 â€‹µV. Females displayed significantly larger ΔPe magnitudes and smaller ΔERN magnitudes than males. Additionally, normative data for behavioral performance (accuracy, post-error slowing, and reaction time) on the Flanker task is reported. Results provide a means by which ERN and Pe amplitudes of young adults elicited by the arrow Flanker task can be benchmarked, facilitating the classification of neural responses as 'large,' 'medium,' or 'small'. The ability to classify responses in this manner is a necessary step towards expanded use of these measures in assessment and research settings. These norms may not apply to ERPs elicited by other tasks, and future work should establish similar norms using other tasks.

Electrophysiological indicators of gesture perception.

Electroencephalography (EEG) activity in the mu frequency band (8-13 Hz) is suppressed during both gesture performance and observation. However, it is not clear if or how particular characteristics within the kinematic execution of gestures map onto dynamic changes in mu activity. Mapping the time course of gesture kinematics onto that of mu activity could help understand which aspects of gestures capture attention and aid in the classification of communicative intent. In this work, we test whether the timing of inflection points within gesture kinematics predicts the occurrence of oscillatory mu activity during passive gesture observation. The timing for salient features of performed gestures in video stimuli was determined by isolating inflection points in the hands' motion trajectories. Participants passively viewed the gesture videos while continuous EEG data was collected. We used wavelet analysis to extract mu oscillations at 11 Hz and at central electrodes and occipital electrodes. We used linear regression to test for associations between the timing of inflection points in motion trajectories and mu oscillations that generalized across gesture stimuli. Separately, we also tested whether inflection point occurrences evoked mu/alpha responses that generalized across participants. Across all gestures and inflection points, and pooled across participants, peaks in 11 Hz EEG waveforms were detected 465 and 535 ms after inflection points at occipital and central electrodes, respectively. A regression model showed that inflection points in the motion trajectories strongly predicted subsequent mu oscillations ([Formula: see text]<0.01); effects were weaker and non-significant for low (17 Hz) and high (21 Hz) beta activity. When segmented by inflection point occurrence rather than stimulus onset and testing participants as a random effect, inflection points evoked mu and beta activity from 308 to 364 ms at central electrodes, and broad activity from 226 to 800 ms at occipital electrodes. The results suggest that inflection points in gesture trajectories elicit coordinated activity in the visual and motor cortices, with prominent activity in the mu/alpha frequency band and extending into the beta frequency band. The time course of activity indicates that visual processing drives subsequent activity in the motor cortex during gesture processing, with a lag of approximately 80 ms.

Reward dysfunction in major depression: multimodal neuroimaging evidence for refining the melancholic phenotype.

Reward dysfunction is thought to play a core role in the pathophysiology of major depressive disorder (MDD). Event-related potential (ERP) and functional magnetic resonance imaging (fMRI) studies have identified reward processing deficits in MDD, but these methods have yet to be applied together in a single MDD sample. We utilized multimodal neuroimaging evidence to examine reward dysfunction in MDD. Further, we explored how neurobiological reward dysfunction would map onto subtypes of MDD. The feedback negativity (FN), an ERP index of reward evaluation, was recorded in 34 unmedicated depressed individuals and 42 never-depressed controls during a laboratory gambling task. Ventral striatal (VS) activation to reward was recorded in a separate fMRI session, using an identical task, among a subgroup of 24 depressed individuals and a comparison group of 18 non-depressed controls. FN amplitude was blunted in MDD. This effect was driven by a MDD subgroup characterized by impaired mood reactivity to positive events, a core feature of melancholic MDD. A similar pattern was observed for VS activation, which was also blunted among the MDD subgroup with impaired mood reactivity. Neither FN amplitude nor VS activation was related to the full, DSM-defined melancholic or atypical MDD subtypes. Across the MDD sample, FN amplitude and VS activation were correlated, indicating convergence across methods. These results indicate that not all MDD is characterized by reward dysfunction, and that there is meaningful heterogeneity in reward processing within MDD. The current study offers neurobiological evidence that impaired mood reactivity is a key phenotypic distinction for subtyping MDD, and further suggests that the existing melancholic phenotype may require further refinement.

When they just don't sleep: differential impacts of reduced child sleep on depression, anxiety, and stress among caregivers of children with and without neurogenetic syndromes.

Introduction: Children with neurogenetic syndromes commonly experience significant and pervasive sleep disturbances, however, associations with caregiver mental health remains unclear. Previous studies have linked sleep disturbances with increased caregiver depression in typically developing populations, and heightened caregiver stress among neurogenetic populations. The present study expands on findings by exploring the longitudinal association between child sleep duration and caregiver mental health (depression, anxiety, stress) throughout development (infancy to school-aged children) in dyads with and without a child affected by a neurogenetic syndrome. Methods: Participants were drawn from the Purdue Early Phenotype Study, including 193 caregivers (Age: M = 34.40 years, SD = 4.53) of children with neurogenetic syndromes (Age: M = 40.91 months, SD =20.72) and typically developing children (n = 55; Age: M = 36.71 months, SD = 20.68). Children in the neurogenetic group were diagnosed with Angelman (n = 49), Prader Willi (n = 30), Williams (n = 51), and Fragile X (n = 8) syndromes. Caregivers completed assessments every six months up to child age three, and annual assessments thereafter. Child sleep duration was measured using the Brief Infant Sleep Questionnaire, and caregiver internalizing symptoms were assessed using the Depression, Anxiety, Stress Scale. Multilevel models were conducted to examine caregiver depression, anxiety, and stress in relation to child sleep duration at both between- and within-person levels, with child age as a moderator. Results: Results indicated a between-person effect of child sleep duration on caregiver depression (i.e., differences between families) and a within-person effect on caregiver stress (i.e., change over time) in the full, combined sample. These effects were not maintained when examined separately in neurogenetic and typically developing groups, except for a between-person effect on caregiver stress in the typically developing cohort. Moderating effects of child age were significant for depression and stress only in the typically developing cohort. Discussion: In summary, persistent child sleep disruptions were linked to exacerbated caregiver depression across the sample, while acute child sleep disruptions exacerbate caregiver stress within dyads over time. These findings emphasize the importance of addressing child sleep to enhance caregiver wellbeing and has potential relevance for a wide range of neurogenetic syndromes.

Abnormal neural sensitivity to rewards as a candidate process of high depression risk in the FMR1 premutation: A pilot study.

The etiological heterogeneity of depression poses a challenge for prevention and intervention efforts. One solution is to map unique etiological pathways for subgroups defined by a singular risk factor. A relevant population for this approach is women who carry the premutation of the fragile X messenger ribonucleoprotein 1 (FMR1) gene, who are at high risk for adult-onset depression. This study explores a candidate neurophysiological marker of depression risk: reduced reward sensitivity, indexed by the reward positivity (RewP). The RewP has been linked to depression risk in the general population, but is unexplored within FMR1 premutation carriers. 16 women with the FMR1 premutation and a matched control group completed a simple guessing task while the electroencephalogram was recorded. Among premutation carriers, RewP difference score (win versus loss) was reduced. These preliminary finding suggest that the FMR1 premutation may confer increased risk for depression in part through abnormal neural sensitivity to rewards.

Error-related brain activity shapes the association between trait neuroticism and internalizing symptomatology in two tasks.

The current study examined how individual differences in error-related brain activity might moderate the association between high trait neuroticism and internalizing symptoms. Data were collected from a sample of high-achieving young adults (N = 188) as part of a larger study on risk versus resiliency for psychopathology. Participants completed two behavioral tasks to elicit the error-related negativity (ERN): an arrow Flanker task and a Go/No-Go task. Analyses were constrained to two internalizing symptom dimensions of checking behavior and irritability. Contrary to expectations, ERN amplitude was not related to symptom severity at the bivariate level. However, ERN amplitude moderated the association between trait neuroticism and symptoms of ill temper, such that the neuroticism-irritability association was strongest among individuals with a blunted ERN. In addition, this finding was relatively consistent across tasks and across two complementary methods of scoring the ERN, suggesting an effect of ERN variance that is shared between tasks and that is relatively robust regarding processing differences. In all, the current study represents the first attempt to investigate how the ERN interacts with trait neuroticism to predict transdiagnostic symptom dimensions in adulthood.

Resting-state EEG power differences in autism spectrum disorder: a systematic review and meta-analysis.

Narrative reviews have described various resting-state EEG power differences in autism across all five canonical frequency bands, with increased power for low and high frequencies and reduced power for middle frequencies. However, these differences have yet to be quantified using effect sizes and probed robustly for consistency, which are critical next steps for clinical translation. Following PRISMA guidelines, we conducted a systematic review of published and gray literature on resting-state EEG power in autism. We performed 10 meta-analyses to synthesize and quantify differences in absolute and relative resting-state delta, theta, alpha, beta, and gamma EEG power in autism. We also conducted moderator analyses to determine whether demographic characteristics, methodological details, and risk-of-bias indicators might account for heterogeneous study effect sizes. Our literature search and study selection processes yielded 41 studies involving 1,246 autistic and 1,455 neurotypical individuals. Meta-analytic models of 135 effect sizes demonstrated that autistic individuals exhibited reduced relative alpha (g = -0.35) and increased gamma (absolute: g = 0.37, relative: g = 1.06) power, but similar delta (absolute: g = 0.06, relative: g = 0.10), theta (absolute: g = -0.03, relative: g = -0.15), absolute alpha (g = -0.17), and beta (absolute: g = 0.01, relative: g = 0.08) power. Substantial heterogeneity in effect sizes was observed across all absolute (I2: 36.1-81.9%) and relative (I2: 64.6-84.4%) frequency bands. Moderator analyses revealed that age, biological sex, IQ, referencing scheme, epoch duration, and use of gold-standard autism diagnostic instruments did not moderate study effect sizes. In contrast, resting-state paradigm type (eyes-closed versus eyes-open) moderated absolute beta, relative delta, and relative alpha power effect sizes, and resting-state recording duration moderated relative alpha power effect sizes. These findings support further investigation of resting-state alpha and gamma power as potential biomarkers for autism.

Neural deficits in anticipatory and consummatory reward processing are uniquely associated with current depressive symptoms during adolescence.

Deficits within the consummatory phase of reward processing are associated with increased depression symptoms and risk; however, few studies have also examined other aspects of reward processing in relation to depression. In the current study, a community sample of 121 adolescents (Mage  = 13.1, Min = 11.14; Max = 15.12; 54% male) completed self-report questionnaires to assess depressive symptoms and the monetary incentive delay (MID) task while EEG was recorded. Results indicated that a reduced cue-P300 as well as a reduced reward positivity (RewP) and feedback negativity (FN) to gain and loss feedback, respectively, were associated with increased depressive symptoms; on the other hand, SPN and feedback P300 were unrelated to depressive symptoms. An exploratory multiple regression analysis revealed that a reduced money cue-P300, a reduced RewP, and a reduced (i.e., less negative) FN, all explained unique variance in depressive symptoms. The current study demonstrates that reduced cue-P300, RewP, and FN amplitudes may reflect distinct deficits in reward processing among adolescents with increased depressive symptoms. Notably, this study is one of the first to leverage the MID task in adolescents in relation to depressive symptoms, allowing for a more in-depth view of the individual differences in reward processing among adolescents with increased depressive symptomatology.

All the Pringle ladies: Neural and behavioral responses to high-calorie food rewards in young adult women.

Reward processing is vital for learning and survival, and can be indexed using the Reward Positivity (RewP), an event-related potential (ERP) component that is larger for rewards than losses. Prior work suggests that heightened motivation to obtain reward, as well as greater reward value, is associated with an enhanced RewP. However, the extent to which internal and external factors modulate neural responses to rewards, and whether such neural responses motivate reward-seeking behavior, remains unclear. The present study investigated whether the degree to which a reward is salient to an individual's current motivational state modulates the RewP, and whether the RewP predicts motivated behaviors, in a sample of 133 women. To elicit the RewP, participants completed a forced-choice food reward guessing task. Data were also collected on food-related behaviors (i.e., type of food chosen, consumption of the food reward) and motivational salience factors (i.e., self-reported hunger, time since last meal, and subjective "liking" of food reward). Results showed that hungrier participants displayed an enhanced RewP compared to less hungry individuals. Further, self-reported snack liking interacted with RewP magnitude to predict behavior, such that when participants reported low levels of snack liking, those with a smaller RewP were more likely to consume their snacks than those with a larger RewP. Our data suggest that food-related motivational state may increase neural sensitivity to food reward in young women, and that neural markers of reward sensitivity might interact with subjective reward liking to predict real-world eating behavior.

Abnormal neurophysiological sensitivity to rewards in depression is moderated by sex and age in middle adulthood.

A candidate pathophysiological process in major depressive disorder is diminished neural reactivity to reward delivery, which is theorized to give rise to anhedonia. Reduced amplitude in the reward positivity (RewP), which captures initial reward evaluation, has been linked to current symptoms of depression among child, adolescent, and young adult samples. However, the developmental trajectory of this association is incomplete, with relatively few studies in middle and older adulthood. Further, emerging evidence in the literature also suggests that this association may be linked to female sex-specific processes, but no studies to date have directly contrasted the effect of sex on the depression-RewP association. The current study sought to address these gaps by testing how sex and age may moderate the depression-RewP association within a mature adult community sample. Symptoms of depression were evaluated using a survey and a clinical interview, and the RewP was elicited using a simple guessing task. There was a three-way interaction between depression symptom severity, age, and sex in predicting RewP amplitude. This was driven by younger (late 30's to early 40's) female-sexed people such that for this group, elevated symptoms of depression were associated with blunting of the RewP. This association tapered around age 50. This effect was specific to clinician-rated rather than self-reported depressive symptom severity. This pattern of effects suggests that among female-sexed people, developmental processes continue to shape the association between reward responsiveness and depression throughout middle adulthood.

An Ethics and Social-Justice Approach to Collecting and Using Demographic Data for Psychological Researchers.

The collection and use of demographic data in psychological sciences has the potential to aid in transforming inequities brought about by unjust social conditions toward equity. However, many current methods surrounding demographic data do not achieve this goal. Some methods function to reduce, but not eliminate, inequities, whereas others may perpetuate harmful stereotypes, invalidate minoritized identities, and exclude key groups from research participation or access to disseminated findings. In this article, we aim to (a) review key ethical and social-justice dilemmas inherent to working with demographic data in psychological research and (b) introduce a framework positioned in ethics and social justice to help psychologists and researchers in social-science fields make thoughtful decisions about the collection and use of demographic data. Although demographic data methods vary across subdisciplines and research topics, we assert that these core issues-and solutions-are relevant to all research within the psychological sciences, including basic and applied research. Our overarching aim is to support key stakeholders in psychology (e.g., researchers, funding agencies, journal editors, peer reviewers) in making ethical and socially-just decisions about the collection, analysis, reporting, interpretation, and dissemination of demographic data.