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Published in final edited form as: J Exp Child Psychol. 2025 Oct 18;262:106398. doi: 10.1016/j.jecp.2025.106398

Parental Anhedonic versus Non-Anhedonic Depressive Symptoms and Children’s Reward Processing

Elana S Israel 1, Brandon E Gibb 1
PMCID: PMC13615874  NIHMSID: NIHMS2203915  PMID: 41110207

Abstract

There is preliminary evidence that children of parents with depression exhibit alterations in reward processing that may increase children’s risk for developing psychopathology (e.g., depression). However, depression is a heterogeneous disorder, and it is unclear whether specific symptoms of depression may be particularly associated with increased risk in children. The current study examined links between parents’ anhedonic versus non-anhedonic symptoms of depression and neural indices of reward outcome processing in children. Participants in this study were a community sample of 217 parent-child dyads (children ages 7–11; 53.00% male, 65.90% non-Hispanic White). Children’s reward outcome processing was assessed during a simple guessing task with the reward positivity (RewP) event-related potential (ERP), which indexes initial neural responsiveness to positive and negative outcome feedback (e.g., winning or losing money). Higher levels of parental anhedonic, but not non-anhedonic, depressive symptoms were associated with more blunted reactivity to both positive and negative outcome feedback in children. The finding was maintained when statistically controlling for children’s own levels of depression and positive affect. These results suggest that parental anhedonia may be a core feature of depression uniquely related to alterations in children’s reward processing, which may have important implications for interventions designed to reduce risk in youth.

Keywords: Reward Positivity, Event-Related Potentials, Anhedonia, Depression, Child

Children of parents who experience depression are at elevated risk of developing psychopathology themselves (Goodman, 2020; Nomura et al., 2002). One hypothesized mechanism of risk is disruptions in children’s reward processing, which could increase children’s risk for depression, substance abuse, and other forms of psychopathology associated with alterations in neural reward circuitry. Although there is some evidence that parental depression is associated with neural indices of reward processing in children (see Kujawa & Burkhouse, 2017; Luking et al., 2016), depression is a highly heterogeneous disorder and it is unclear whether certain symptom domains may be particularly important in understanding children’s risk.

According to the tripartite model (Clark & Watson, 1991), depression is composed of a cluster of symptoms reflecting broad negative affect/general distress as well as symptoms of anhedonia (reduced interest or pleasure) and theorists have proposed that anhedonia is the core feature of depression associated with reward processing (Admon & Pizzagalli, 2015). Importantly, anhedonia has been shown to be uniquely associated with a host of negative outcomes such as more severe depressive episodes, increased risk for suicidality, and greater resistance to traditional treatments for depression (for reviews see Pizzagalli, 2022; Serretti, 2023) and, as such, is important to investigate independently from overall depression diagnosis status. Consistent with the National Institute of Mental Health (NIMH) Research Domain Criteria (RDoC) initiative (Insel et al., 2010) and developmental psychopathology more broadly (Cicchetti, 1984), it is also important to examine potential influences (and outcomes) dimensionally rather than only categorically (presence versus absence of a diagnosis). To date, however, no studies have examined links between parental anhedonia specifically and children’s reward processing. This type of investigation is important because it could provide a better understanding of potential developmental contributors to aberrant reward processing, which could be used to inform more targeted prevention efforts.

To address this gap, we examined links between parents’ levels of anhedonia and neural markers of reward outcome processing in children. In doing so, we focused on the reward positivity (RewP) event-related potential (ERP) component, which indexes initial neural responses to outcome feedback (e.g., winning or losing money; Glazer et al., 2018; Proudfit, 2015). A more blunted RewP has been shown to be associated with depression risk status (e.g., having a parental history of depression; Freeman et al., 2022; Kujawa et al., 2014), future depression in youth (Hoang et al., 2025; Mackin et al., 2023) and there is some evidence that it may relate to anhedonia symptoms in youth (Szenczy et al., 2025), supporting its use as a biomarker for depression risk. We hypothesized that higher levels of parental anhedonia would be related to reduced reward responsiveness among children. We also predicted that parents’ symptoms of anhedonia would be more strongly related to children’s reward processing than parents’ non-anhedonic symptoms of depression. Exploratory analyses examined whether any of the observed relations were moderated by children’s demographic characteristics (age, sex, race/ethnicity) to potentially identify subgroups at particularly high risk. Finally, to determine whether any observed relations were at least partially independent of children’s own symptoms, sensitivity analyses examined whether significant findings were maintained when statistically controlling for children’s levels of depression and positive affect, as low positive affect is thought to be related to experiences of anhedonia.

Method

Participants and Procedure

Participants were 217 parent-child dyads recruited from the community using a variety of means to maximize reach (e.g., social media, newspaper ads, bus ads, etc.). Given that the goal of the parent study was to include a representative community sample, the only inclusion/exclusion criteria were that children be 7–11 years old and not have a developmental or learning disability, per their parent’s report, that would prevent them from completing the study procedures. This age range was selected because we aimed to examine markers of depression risk during the developmental period preceding adolescence when rates of MDD start to increase significantly. For this current study, we excluded parents if they had a lifetime history of bipolar disorder or a psychotic disorder because we aimed to examine children’s reward processing in the context of depression risk specifically.

Of the original sample of 257 children, 15 were excluded for having another sibling in the study to preserve independence of observations. An additional 25 children were excluded for having an insufficient number of useable trials for the Doors task (described below). The final sample, therefore, included 217 children and their parent. Included and excluded dyads did not differ significantly on any study variable. The average age of children was 9.68 (SD = 1.41) and 53.00% were male. Of the children, 10.19% were Hispanic, 65.90% were non-Hispanic White, 12.90% were non-Hispanic Black/African American, 11.06% were multiracial, and the remainder were from another racial group. The average age of parents was 38.00 (SD = 6.31) and 88.48% were female (86.64% biological mothers; 11.06% biological fathers; 2.30% other caregivers). Of the parents, 5.53% were Hispanic, 76.96% were non-Hispanic White, 14.74% were non-Hispanic Black/African American, and the remainder were from another racial group. The median household income for participating families was between $40,000-$45,000. Based on 2014 census data from the county in which this study took place, this sample had a lower median household income ($40,000-$45,000 compared to $50,849) and was more racially and ethnically diverse (76.96% of parents and 65.90% of children non-Hispanic White compared to 84.8% non-Hispanic White; U.S Census Bureau, n.d.). As part of the larger study, parents’ and children’s histories of major depressive disorder (MDD) were assessed with the Structured Clinical Interview for DSM-IV Axis I Disorders (SCID-IV; First et al., 2002) and the Schedule for Affective Disorders and Schizophrenia for School-Age Children (K-SADS; Kaufman et al., 1997). Although our primary focus was on parents’ levels of anhedonia, we report rates of current MDD in parents and children to characterize the sample more fully. Ten (4.61%) of the parents and 2 (0.92%) of the children met criteria for current MDD.

Following informed consent/assent, parents and children completed questionnaires and then children completed the Doors Task (described below). All study procedures were approved by the university’s Institutional Review Board.

Measures

Reward Processing

Reward Task.

The Doors Task was used to assess reward outcome processing in response to gaining or losing money (Proudfit, 2015). During this task, participants are presented with two doors side-by-side and are instructed to choose which door has a prize behind it. They are told that if they guess correctly, they will win $0.50 and if they guess incorrectly, they will lose $0.25. The task consisted of 50 trials with 25 gain trials and 25 loss trials presented in a random order. All participants received $5 after completing the task.

EEG Data Acquisition and Processing.

During the Doors Task, continuous EEG was recorded using a BioSemi ActiveTwo system with 34 scalp electrodes. Electrooculogram electrodes were used for the inspection of eye movements. Data were digitized at a 24-bit resolution with a sampling rate of 512 Hz and were re-referenced to the average of the left and right mastoid electrodes. Band-pass filters were applied with cut-offs of 0.1 and 30 Hz using a second-order IIR Butterworth filter with a 12 dB/octave roll-off. Independent component analysis (ICA) was used for artifact rejection and correction (Jung et al., 2001). Data were segmented into epochs beginning 200 ms before the onset of the feedback stimulus and ending 1000 ms after the onset of the stimulus and were baseline corrected. Trials that contained large artifacts (>100 μV) were removed and participants who had less than 14 trials per gain/loss condition were excluded. Because reward outcome processing consists of several substages unfolding rapidly within the first second following feedback, each indexed by ERP components that overlap temporally and spatially (Glazer et al., 2018), we used principal component analysis (PCA) to isolate neural activity consistent with features of the RewP (see Figure 1; Dien, 2012). The PCA factor that was most consistent with the RewP peaked at 320 milliseconds at electrode Cz. For more detailed information about the EEG data acquisition, processing, and PCA, see Gibb et al. (2022).

Figure 1. Temporospatial factor consistent with RewP characteristics. Panel A presents the ERP waveform and panel B presents the scalp map at the one millisecond peak.

Figure 1.

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Parent Symptoms

Parents’ symptoms were assessed using the Mood and Anxiety Symptom Questionnaire-Short Form (Clark & Watson, 1991; Watson, Clark, et al., 1995; Watson, Weber, et al., 1995). We focused on the Anhedonic Depression (MASQ-AD) and General Distress Depression (MASQ-GDD) subscales, which allowed us to examine anhedonic and non-anhedonic symptoms of depression separately. The MASQ-AD consists of 22 items with possible scores ranging from 22 to 110 with higher scores indicating higher levels of anhedonia symptoms. The MASQ-GDD consists of 12 items ranging from 12 to 60 with higher scores reflecting greater non-anhedonic depressive symptoms. Participants were asked to indicate how they were feeling over the past week. Previous studies have supported the reliability and validity of both subscales (Watson, Clark, et al., 1995; Watson, Weber, et al., 1995). In the current sample, the MASQ-AD and MASQ-GDD demonstrated good internal consistency (α = .85 and .93, respectively). Scores in this sample ranged from 29 to 100 with a mean of 62.08 (SD = 12.39) for the MASQ-AD and 12 to 56 with a mean of 19.52 (SD = 8.68) for the MASQ-GDD.

Child Symptoms

Children’s depression symptoms were assessed using the Children’s Depression Inventory (CDI; Kovacs, 1981). The CDI consists of 27 items, each rated on a 3-point scale, and children are were asked to indicate how they were feeling over the past two weeks, with higher scores indicating more depressive symptoms. Previous research has demonstrated strong reliability and validity of the CDI in children from the community (e.g., Smucker et al., 1986) and it showed good internal consistency in this sample (α = .79). CDI scores ranged from 0 to 30 with a mean of 5.32 (SD = 4.65).

To assess children’s experiences of positive affect, we used the Positive and Negative Affect Schedule for Children—Positive Affect subscale (PANAS-PA; Laurent et al., 1999). The PANAS-PA consists of 12 items and children were instructed to answer how much they experienced each item during the previous few weeks on a 5-point scale from “not at all” to “a lot,” with higher scores indicating more positive affect. Previous research has supported the psychometric properties of the PANAS-PA (Laurent et al., 1999) and it demonstrated good internal consistency in this sample (α = .81). PANAS-PA scores ranged from 20 to 60 (M = 47.20; SD = 7.67).

Analysis Plan

To test our hypotheses, we used repeated measures general linear models (GLMs) with parent symptoms (MASQ-AD or MASQ-GDD) entered as a continuous between-subjects predictor, feedback type (gain, loss) as the within-subject predictor, and children’s RewP amplitude as the outcome. For sensitivity analyses, child measures (CDI and PANAS-PA) were added separately as covariates to the previous analyses to determine whether any significant relations observed remained significant after statistically controlling for these variables.

Results

Preliminary analyses revealed that the MASQ-GDD, CDI, and PANAS-PA, but not the MASQ-AD, showed significant skew. We transformed these variables (using inverse for the MASQ-GDD and square root transformations for the CDI and PANAS-PA) to meet assumptions of normality prior to further analysis.

Focusing first on parent’s MASQ-AD scores, there was a significant main effect of MASQ-AD across feedback type, F(1, 215) = 4.17, p = .04, ηp2 = .02. However, the MASQ-AD × feedback interaction was not significant, F(1, 215) = 0.56, p = .46, ηp2 = .003. Given this, we created a composite RewP gain/loss score (gain and loss amplitudes added together) and found that higher MASQ-AD scores were associated with more blunted RewP amplitudes across feedback type, r = −.14, p = .04. Turning next to MASQ-GDD scores, neither the main effect of MASQ-GDD, F(1, 215) = 0.06, p = .81, ηp2 = .00, nor the MASQ-GDD × feedback type interaction, F(1, 215) = 1.72, p = .19, ηp2 = .008, was significant.1 In addition, the relation between MASQ-AD and RewP amplitudes (collapsing across feedback type) was significantly stronger than the relation between MASQ-GDD and RewP amplitudes (rs = −.14 vs. −.02; z = −2.05, p = .04) further supporting the specificity to parents’ anhedonia. Sensitivity analyses also showed that, even after statistically controlling for children’s CDI and PANAS-PA levels, the relation between MASQ-AD children’s RewP (collapsing across gain and loss feedback) remained significant (highest p = .05).

Finally, we conducted exploratory analyses to examine whether the relation between MASQ-AD and RewP was moderated by child demographic characteristics (age, sex, and race/ethnicity). The MASQ-AD × child race/ethnicity interaction was a nonsignificant trend, F(1, 213) = 3.33, p = .07, ηp2 = .02 (all other ps > .10). Although not statistically significant, the form of this interaction was such that higher MASQ-AD scores were associated with more blunted RewP amplitudes (across gains and losses) among children from marginalized racial/ethnic groups, r = −.30, p = .01, but not among non-Hispanic White children, r = −.03, p = .72.

Discussion

The goal of this study was to extend prior research examining the link between parental depression and children’s reward outcome processing, focusing specifically on parents’ symptoms of anhedonia versus non-anhedonic depressive symptoms. As predicted, higher levels of parental anhedonia were associated with reduced neural reactivity to monetary reward outcome feedback, and this relation was significantly stronger for parents’ anhedonia compared to non-anhedonic symptoms of depression. It should be noted that effect sizes for our findings were small which may be due to our sample being relatively young and the potential presence of moderators (e.g., race/ethnicity as discussed below), which may further specify groups at particular risk for reward dysfunction. There were no significant interactions with feedback type, suggesting that higher levels of parental anhedonia are related to blunted neural responses to both positive and negative outcome feedback in children. Consistent with theories positing that individuals with depression experience general blunted engagement with both positive and negative aspects of the environment (e.g., emotion context insensitivity theory; Rottenberg et al., 2005), it is possible that children of parents with heightened anhedonia have reduced reactivity to general feedback, irrespective of valence.

Interestingly, there was a non-significant trend of child race/ethnicity moderating the association between parents’ anhedonia and the RewP where children from marginalized racial/ethnic backgrounds showed a significant relation and White children did not. Although this should be interpreted cautiously, it is possible that children from marginalized racial/ethnic groups, who often encounter increased stressors in their lives, are more vulnerable to the effects of parental anhedonia at the neural level. However, future is research is needed to determine if this finding is observed in other samples.

This is the first study to show that parental anhedonia, a core feature of depression, is associated with alterations in children’s neural reward processing. These results extend previous research showing that parents’ history of major depression relates to youth’s reward processing (Kujawa & Burkhouse, 2017; Luking et al., 2016) by starting to unpack the heterogeneity of depression and demonstrating that parents’ anhedonia is more strongly related to children’s reward responsiveness than non-anhedonic symptoms of depression. Our findings suggest that identifying a specific symptom profile that is theoretically and empirically linked with children’s reward processing, rather than examining depression categorically, may be important in providing a more fine-grained understanding of how parental psychopathology contributes to risk in children. This type of investigation aligns with research initiatives that focus on underlying symptom mechanisms rather than discrete disorders (e.g, RDoC; Insel et al., 2010). In other words, perhaps studying how specific domains of functioning (e.g., the positive valence system) relate to neurobiological markers that are thought to underly this type of functioning could clarify mechanisms of risk. Therefore, future research should investigate how other measures of parental anhedonia (e.g., self-report, neural, behavioral, etc.) relate to children’s reward processing. Importantly, the current findings support the use of preventative interventions for at-risk youth that focus on increasing positive affect among families (e.g., Burkhouse et al., 2023).

This study had several strengths including a large and diverse sample and the use of an objective neural measure of reward responsiveness. However, there were also limitations that present avenues for future research. First, this study focused on children and reward sensitivity typically peaks during adolescence (Galvan, 2010; Urošević et al., 2012). Therefore, future research should replicate these findings in a slightly older adolescent sample and examine whether children’s blunted reward processing mediates the relation between parental anhedonia and future depression during adolescence. Second, our task focused on responses to monetary reward outcome feedback and future research is needed to examine links between parental anhedonia and different stages of the reward process (e.g., reward anticipation) as well as processing of other types of reward (e.g., peer acceptance and rejection). Alterations in both monetary and social reward processing has been linked to depression risk in youth (see Luking et al., 2016) and it remains unclear whether one may be a better predictor of risk and more strongly relate to parental anhedonia. Finally, although we included all types of caregivers in this sample, participating caregivers tended to be biological mothers and we are likely underpowered to detect differences between caregiver type. Future research should examine whether there are differences in the link between caregiver anhedonia (e.g., mothers vs. fathers) and children’s reward processing.

In summary, the results of this study support the link between parental anhedonia and children’s neural reward outcome processing. These findings may have important implications for identifying youth who may be most at risk of developing disorders related to reduced reward functioning (e.g., depression, substance misuse) and highlight the need to assess parents’ symptoms of anhedonia specifically, rather than only depression more broadly. Ultimately, this line of research could inform detection and prevention efforts for youth psychopathology.

Supplementary Material

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Highlights.

  • Parental anhedonia is related to reduced reward responsivity in children

  • Non-anhedonic depressive symptoms were not related to reward processing

  • These findings may help to identify children most at risk for psychopathology

Funding Sources

This project was supported by National Institute of Mental Health grants MH135649 (EI), MH098060 (BG), and MH130397 (BG). The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health.

The authors would like to thank Devra Alper, Katie Burkhouse, Eric Funk, Andrea Hanley, Kiera James, Anastacia Kudinova, Cope Feurer, Aliona Tsypes, Sydney Meadows, Effua Sosoo, Michael Van Wie, and Mary Woody for their help in conducting assessments for this project.

Footnotes

Declarations

The authors have no competing or potential conflicts of interest.

Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.

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Although we focused on the PCA-derived RewP to isolate the RewP from other temporally and spatially overlapping substages of reward outcome processing, we also examined the mean amplitude-based RewP (average amplitude 275–375 ms after feedback at FCz) for interested readers. As expected, results were weaker with the mean amplitude-based RewP. Additional details of these analyses are available in the supplemental materials.

Availability of data

Data reported in this article are available upon request from the corresponding author.

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Associated Data

This section collects any data citations, data availability statements, or supplementary materials included in this article.

Supplementary Materials

1
NIHMS2203915-supplement-1.docx (101.5KB, docx)

Data Availability Statement

Data reported in this article are available upon request from the corresponding author.

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