Your new experience awaits. Try the new design now and help us make it even better

REVIEW article

Front. Psychiatry, 19 September 2025

Sec. Perinatal Psychiatry

Volume 16 - 2025 | https://doi.org/10.3389/fpsyt.2025.1663017

This article is part of the Research TopicWomen in Psychiatry 2024: Perinatal PsychiatryView all 7 articles

Executive functioning in matrescence and implications for perinatal depression

T. Roxana Ghadimi*T. Roxana Ghadimi*Clare McCormack*Clare McCormack*
  • Department of Child and Adolescent Psychiatry, New York University (NYU) Grossman School of Medicine, New York, NY, United States

The perinatal period represents a time of profound neurobiological, cognitive, and emotional change. While evidence points to the neuroplasticity of matrescence as adaptive in supporting the transition to motherhood, the perinatal period also entails subjective reports of cognitive difficulty known as “mommy brain” as well as a heightened vulnerability to mental health challenges. The role of cognition in the etiology of postpartum depression is a promising area of investigation into targets for maternal mental health intervention, considering evidence that important cognitive changes occur during the perinatal period, and given that cognitive alterations are key features of mood disorders. Here we review evidence for cognitive plasticity in matrescence, with a particular focus on executive function (EF) given its overlapping significance for adaptation to parenthood, central role in managing the mental load of motherhood, and implications in mood regulation and mood disorders. We also review evidence for EF changes in perinatal depression and major depressive disorder more broadly. Despite the strong association between EF impairments and major depressive disorder, research on EF changes in perinatal depression remains limited. Understanding normative EF changes during this period is essential for better understanding the relationship between EF, perinatal depression, and the mental load of motherhood. Consideration for these cognitive, neurobiological, and psychosocial factors of matrescence is critical for addressing maternal mental health and developing interventions that support parental well-being.

1 Introduction

In two recent health advisories and calls to action, the U.S. Surgeon General highlighted the need to improve the physical and mental health of mothers and mothers-to-be, as well as reduce the burden of parental stress (1, 2). This reflects the seriousness of challenges facing women across the perinatal period and an urgent unmet need. Perinatal mood and anxiety disorders (PMADs) are the most common birth complication, with perinatal depression affecting approximately 1-in 7 mothers and disproportionately impacting women of color (35). PMADs have serious consequences for both mother and baby via associations with preterm birth, compromised parenting quality, maternal substance use and suicide, and long-term impairments in infant and child cognitive social-emotional development, behavior, and family functioning (68). Severe postpartum mental illness can be tragic: the leading cause of pregnancy-related deaths is mental health conditions (22.7%), including from suicides and overdose related to substance use disorders (9). The need for enhanced prevention and treatment for PMADs is therefore urgent. The role of cognition in PMAD etiology is a promising area of investigation into targets for PMAD intervention, considering evidence that important cognitive changes occur during the perinatal period, and given that cognitive and information processing alterations are key features of mood disorders. Here we review evidence for cognitive plasticity in matrescence, with a particular focus on executive function (EF) given its overlapping significance for adaptation to parenthood and in mood regulation. To bridge what is known about cognitive endophenotypes of depression within and beyond the perinatal period, this review will highlight key findings from current research on cognitive changes in mood disorders across matrescence. Because data in the perinatal period is limited, we will supplement with what is known about cognition in major depressive disorder and extrapolate how the relationship between cognition and mood may present in perinatal depression. We will also explore the emerging concept of “the mental load of motherhood” as a unique stressor that is likely taxing a mother’s cognitive capacity and contributing to vulnerability to mental illness throughout matrescence.

2 Neuroplasticity in matrescence

Matrescence is a term coined by anthropologist Dana Raphael in the 1970s to describe the transition to becoming a mother (10). This transformative process of adaptation to the new role and responsibility of caring for young involves profound hormonal, physiological, psychological, and social changes. The hormones of pregnancy, birth, and lactation drive rapid and extreme physiological transformations that are unparalleled across the lifespan (1114). Alongside these changes, the maternal brain undergoes significant structural and functional neuroplasticity (14). Neurobehavioral plasticity throughout matrescence may usher in adaptive changes to support a mother in her new role as caregiver, such as by priming attention and motivation to be directed towards infant cues, and altered information processing in preparation for new demands and increased mental load of parenting (14). When viewed through this lens, perinatal cognitive and neural plasticity represents an overall adaptation to caregiving experiences that facilitates learning the skills of parenting and coping with a new set of challenging demands (15). These adaptations are underscored by evolutionarily conserved plasticity in brain structures that are part of a global “parental caregiving networking” that support mammalian caregiving, including sensitivity to infant cues and infant-parent biobehavioral synchrony (15).

Foundational studies in rodents have demonstrated significant neural plasticity in the peripartum period including alterations in neurogenesis, neuronal morphology, and synaptic plasticity throughout the brain, particularly within the hippocampus, prefrontal cortex, basolateral amygdala, nucleus accumbens, and hypothalamus (13, 16, 17) A small but growing body of evidence has demonstrated that primiparous women undergo extensive and highly consistent reductions in regional gray matter volumes across pregnancy, with pronounced reductions in the entire brain present in the early postpartum compared with preconception (18). These gray matter reductions persist for at least two years after delivery (18). While the whole brain appears affected, anatomical changes appear especially pronounced in prefrontal regions associated with the Default Mode and Frontoparietal Networks, including the medial frontal cortex, precuneus, posterior cingulate cortex, inferior frontal gyri, and superior temporal sulci (1820). The first studies to examine brain change underway during pregnancy have emerged only recently: data suggests a clear linear decrease in gray matter volume beginning early in pregnancy, with a sudden shift in direction after delivery where volumetric gains are observed (1921). Evidence so far of this “fine tuning” of the maternal brain across the perinatal period has been interpreted as adaptive for caregiving and other postpartum behaviors, given that the degree of anatomical change is positively associated with measures of postpartum attachment, and that data so far demonstrates a remarkably consistent trajectory of neural anatomical change in healthy women (18, 22). Given the centrality of prefrontal regions to Theory of Mind (ToM) processes and the importance of these abilities in sensitive caregiving, it might be expected that enhanced ToM ability is a cognitive mediator of anatomical change in prefrontal regions with caregiving behavior, though this remains a gap in literature (22, 23). As the neuroscience of matrescence continues to unfold, examination of how neural functional, anatomical changes, cognitive shifts, and mood symptoms interact will lead to insights into how these neurobiological changes may facilitate the transition to parenthood. In particular, studies in large samples examining individual differences in perinatal neuroplasticity are needed to understand how these potentially influence vulnerability to psychiatric disorders (24, 25).

3 The link between cognition and emotion

Cognitive function has long been linked to emotional health. The ‘emotional brain’ and the ‘cognitive brain’ cannot be separated, as there is significant overlap and interactive effects among neural networks (26). Executive function (EF) is an umbrella term for higher-order cognitive processes mediated by the frontal cortex that are essential for goal-directed behavior. EF includes attention, planning, cognitive flexibility (shifting between ideas), multi-tasking, problem-solving, cognitive inhibition, abstraction, and working memory (27, 28). EF plays an important role in facilitating emotion regulation via inhibitory control, particularly impulse control in the context of both positive and negative emotion (29). Research has suggested that strong inhibitory control is foundational to effective emotion regulation, which is the ability to modulate emotional responses in a flexible and adaptive way (30). Emotion regulation has been increasingly integrated into models of psychopathology, and difficulties with emotion regulation are a core feature of mood disorders including depression, anxiety, and bipolar disorder (31, 32). Enhancing emotion regulation strategies is a target for clinical intervention, as strategies such as reappraisal and acceptance are significantly positively related with well-being (33).

Human parenting is a complex task and requires high-order executive functioning and effective emotional regulation to facilitate sensitive caregiving and parental coping and adaptation (34, 35). Parenting requires a balance between effectively and promptly attending to and responding to infant cues, while maintaining a regulated state in order to sensitively respond to infant needs (34). Processing of infant distress cues are particularly salient, which are inherently emotionally evocative and draw on emotion regulation capacities of parents (36). Accordingly, new mothers show enhanced neural activation in the emotional regulation and cognitive control circuit, with prefrontal cortex activation in response to infant distress cues serving to regulate amygdala activation in the face of negative infant stimuli (37). Further, effective emotion regulation affects the health and wellbeing of both mother and baby. Children may learn to regulate their emotions by employing comparable regulatory approaches of their parents, which may lead to the transmission of adaptive as well as maladaptive regulation skills (34, 3840). Given the bidirectional, dyadic nature of maternal-child mental health, this may in turn have a further positive impact on maternal mood as effective child self-regulation lessens parenting burden. Overall, emotion regulation plays an essential role in a mother’s psychological health as she navigates the responsibilities and demands of motherhood.

3.1 Cognitive shifts in matrescence

Despite the overall adaptive role of cognitive and behavioral changes across matrescence, subjective pregnancy-related cognitive deficits are common anecdotally, and perpetuate the negative concept of “mommy brain.” (41) Studies using self-report measures have found that between 50% to 80% of pregnant women report subjective cognitive complaints or memory difficulties, measured using brief self-report questionnaire items or qualitative methods (4246). However, subjective reports of cognitive complaints are often at odds with performance data from objective cognitive measures. Studies that objectively measured memory performance using standardized assessments show only small differences between perinatal and control groups, primarily concentrated on prefrontally-mediated domains such as working memory performance (27, 41, 43, 4749). These included a broad range of standardized neuropsychological measures commonly used to evaluate EF and cognition, such as the Color-Word Stroop Task, the WAIS-III Digit Symbol Task, the Backward Digit Span Test, and verbal paired associates task (27, 4952). The small differences demonstrated on objective cognitive measures likely do not translate into clinically meaningful differences in function, but may result in greater effort involved in these cognitive processes, contributing to subjective mental fogginess. Furthermore, it is important to distinguish normative cognitive variations associated with the transition to parenthood from deficits that meet the threshold of clinical concern. Mild, transient cognitive changes typically do not interfere with daily functioning, quality of life, or parenting capacity and therefore likely do not constitute a clinically significant cognitive “deficit” or “impairment” beyond what would be expected in a major life adaptation (53, 54).

While the term “mommy brain” is often associated with memory difficulty, the phenomenon may reflect broader executive function changes, as memory requires executive functions including attention, cognitive flexibility, and the ability to distinguish salient information to remember. However, research on perinatal changes in executive functioning remain limited. One meta-analysis found that in the third trimester of pregnancy, women experience deficits in general cognitive function, memory, and executive function, but not during prior trimesters and in non-pregnant controls (27). The findings in this meta-analysis should be interpreted with caution given the small to moderate effect sizes of the differences, medium to high heterogeneity, and the limited number of longitudinal studies available. While findings indicate noticeable but minor cognitive changes, significant impairments in complex tasks appeared less likely, and performance generally fell within normal ranges (27). Another meta-analysis presented results consistent with this finding, also reporting that differences in cognition associated with pregnancy tend to be small and concentrated on specific tasks that tax executive function (49). Specifically, memory measures that place relatively high demands on executive cognitive control and effortful processing, such as free recall (6 independent studies; total N = 419) and executive components of working memory (4 independent studies; total N = 211) appeared to be selectively disrupted (49). The decrement was relatively subtle, and the same specific deficits associated with pregnancy were also observed postpartum (49). These findings point to how the perinatal period may be a time of heightened sensitivity to demands on executive cognitive control, or a heightened mental load. However, studies included in this meta-analysis exhibited high heterogeneity, with much of the variability attributed to the included measures tapping different aspects of memory, as well as sampling error from the small sample sizes in individual studies. There also remain gaps in knowledge about the role of parity and whether the observed cognitive changes mirror those seen in neurological or psychiatric disorders. Further longitudinal research with consistent methodologies is needed to clarify the progression and real-life impact of these cognitive changes during pregnancy.

Executive functioning in the perinatal period deserves particular attention due to its crucial role in parenting, its association with psychiatric disorders, and its vulnerability to environmental demands. Notably, in a small cross-sectional study (N = 85), it was found that when objective memory testing was conducted in a home environment, pregnant women performed worse on prospective memory tasks than non-pregnant controls (55). This finding highlights the impact of the home environment on executive functioning, as prospective memory is a process that relies heavily on executive cognitive control and refers to the ability to remember and execute intended actions at a later time. The finding that executive functioning may be worse in the home environment is likely due to the presence of competing demands and distractions that are absent in a controlled laboratory environment. Though majority of the pregnant women in this study were primiparous, mothers with other young children at home face even more distractions, increased responsibilities, and a generally higher mental load. Thus, the heightened executive function demands of parenting, especially in the home environment, may contribute to cognitive challenges. In fact, mothers have reported that interruptions, cognitive overload, and newfound anxieties are core components of the experience of “mommy brain.” (56) As such, the concept of the mental load of motherhood is important to consider as either a cause or consequence of the overloaded “mommy brain.” Executive function may represent a nexus between neurobiological changes and social determinants of maternal mental health.

3.2 Executive function in postpartum depression

Given the role of EF in adapting to the demands of parenthood, changes in EF may be particularly significant in the context of postpartum depression (PPD), where cognitive and emotional disruptions impact the responsibilities of caregiving. PPD falls within the umbrella of perinatal depression, which is defined in the DSM-V as a major depressive disorder that occurs during pregnancy or within four weeks after giving birth (57). However, it has been recommended that this criterion be extended to 6 months after delivery (58). Deficits in executive function in the postpartum period can have significant impact as they impair a mother’s ability to care for both herself and her child. This can compound challenges associated with mental illness and have enduring effects on mother–infant interactions and child development (6, 7). Despite the prevalence and impact of perinatal mental illness on both mother and child, understanding of the neural mechanisms underpinning peripartum depression and associated cognitive endophenotypes remains limited.

A small but growing body of research highlights a unique neurobiology of perinatal mental illness that involves an interplay of reproductive hormones, oxytocin, inflammation, the kynurenine pathway, genetic factors, and stress (59). Neuroimaging studies indicate differences between women with PPD and controls in functional connectivity in regions of the brain that overlap with the “caregiving network” (60). Functional neuroimaging studies have shown PPD to be associated with altered activity patterns both at rest and in response to specific emotional cues in brain regions involved in executive functioning, including the dorsal medial prefrontal cortex, orbital frontal cortex, and superior frontal gyrus (61, 62). These regions are critical for self-regulation, decision-making, empathy and emotional processing, functions necessary for managing the complex demands of motherhood. While neuroimaging studies have identified functional alternations in brain regions involved in EF among women with PPD, it remains unclear how these neural changes translate to measurable deficits in neuropsychological performance, underscoring the need for studies that directly link brain function to executive functioning task outcomes.

Few studies have directly examined associations between PPD and EF. One cross-sectional study, involving a larger sample than previous in the literature (N = 395), assessed working and short-term memories in mothers and fathers and found that both mothers and fathers with postpartum depression performed worse in a working memory test (63). Notably, the participants were assessed in home visits, where cognitive demands of the home environment may have amplified any cognitive vulnerability associated with PPD. This approach enhances ecological validity and highlights how a high mental load in parenthood may be especially difficult for individuals struggling with PPD. Pregnancy-related depression and anxiety symptoms in mid-pregnancy have been associated with significantly more errors in a visuospatial working memory and executive function task, compared to performance in mothers with low psychiatric symptom levels (64). This finding suggests that EF impairments associated with perinatal depression could impact a mother’s ability to manage the complex demands of caregiving, potentially leading to further stress and worsening mood symptoms. Another cross-sectional study compared executive functioning in third-trimester pregnant women with depressive symptoms to those without depressive symptoms, finding worse cognitive inhibition performance in women with depressive symptoms (65). This finding has implications for emotion regulation, as cognitive inhibition allows for suppression of and a shifting away from negative thoughts in order to regulate emotions. As such, there may be a positive feedback loop between depressive symptoms, impaired cognitive inhibition, and further affective dysregulation. It remains unknown whether EF decrements serve as a risk factor for PPD or whether the cognitive demands of early parenthood exacerbate existing vulnerabilities.

There remains an opportunity to further investigate the neurocognitive profile of PPD, drawing on approaches from studies of cognitive endophenotypes in non-pregnant populations. Cognitive endophenotypes are measurable aspects of cognition that serve as intermediate markers linking risk factors to psychiatric conditions or may represent a prodromal state. For example, a prominent endophenotype in bipolar disorder seems to be a response inhibition deficit, a potential marker of ventral prefrontal dysfunction (66). In major depressive disorder (MDD), impairments in executive cognitive function including selecting strategies, planning, and monitoring performance) are seen, though are not specific for MDD (67). These cognitive endophenotypes may offer valuable insight into how shifts in executive function and related neural mechanisms may impact or predict mood disorders in the perinatal period.

More research is needed to better understand cognitive endophenotypes for PMADs. Because research into cognitive endophenotypes in the perinatal period is relatively scarce, understanding what it known about neuropsychological deficits, specifically executive functioning in MDD outside of pregnancy, may provide important insights into perinatal cognitive endophenotypes.

3.3 Executive functioning in major depressive disorder

MDD is associated with cognitive deficits, particularly in EF, memory, and attention. A cognitive model of depression suggest that impaired cognition plays a crucial role in the onset and maintenance of depression by reinforcing negative information processing biases (68). The cognitive neuropsychological model of depression also suggests that treatments for MDD exert their beneficial effects by alleviating these biases (69). Functional neuroimaging studies have linked executive dysfunction in MDD to altered activity in prefrontal executive networks during common cognitive performance tasks (7072). Specifically, there is evidence for alterations in key emotion regulatory regions, including abnormally increased activity in the dorsolateral (dlPFC) and ventrolateral prefrontal cortex (vlPFC) and decreased activity in the dorsal anterior cingulate cortex (dACC) (72). Therefore, even in the absence of meaningful differences in performance, there may be aberrant patterns of brain activation during executive tasks among depressed populations. Whether the same is true in PPD specifically is not clear.

Cognitive deficits are a well-documented aspect of MDD, affecting executive function, working memory, attention, and learning (73). One meta-analysis demonstrated that MDD is consistently linked to worse performance on neuropsychological measures of EF, with moderate to substantial effect sizes (74). There is strong evidence for impairment in processing speed, learning, and memory in an acute depressive episode (73). These deficits have been found to be more pronounced in individuals experiencing more severe symptoms and those on psychotropic medications (74). Depressed patients require greater cognitive effort and longer cognitive processing time to execute executive functioning tasks (75). Impaired cognition occurs in around two-thirds of depressed patients (76) and persists beyond acute episodes. Individuals with MDD, even in remission, exhibited moderate deficits in EF and attention, with smaller but persistent impairments in memory (77). About one-third to one-half of remitted depressed patients are thought to be affected by cognitive deficits (78, 79). Evidence from another meta-analysis indicates that the deficits that remain in remission are more mild than in acute episodes, and include working memory, attention, and learning and memory functions (73). Cognitive impairments in depression contribute to its chronicity, treatment resistance, and functional burden (69, 80). While more research is needed to determine the casual relationship between MDD and cognitive dysfunction (81), it presents a promising paradigm that could be applied to PPD.

3.4 Understanding the cognitive burden of motherhood: Interactions between mental load and executive function

The concept of mental load captures the cognitive demands placed on an individual when performing tasks or processing information (8285). It encompasses the mental effort and resources required to manage and complete various cognitive activities and can be seen as the “cost” of mental labor on the limited mental capacity of an individual (84). Mental overload has been defined as a mismatch between task demands and available resources (85). Findings in domains outside of parenting emphasize the role of executive function in managing and perceiving mental load and hold implications for how cognitive resources are allocated in complex, multitasking environments (86). In parenting, if the demands of this cognitive and emotional labor exceed a parent’s ability to cope, parents may experience cognitive overwhelm, emotional strain, reduced cognitive and emotional resources for bonding, and taxed executive functions. A limiting factor in this field is the current lack of validated instruments for measuring mental load of parenting, in part due to the complexity of measuring this phenomenon outside of constrained laboratory-based tasks, where the concept originated (83, 8789). Despite this challenge, an integration of cognitive and social dimensions of mental load provide a useful framework for understanding how matrescence may tax cognitive resources. The term “The Mental Load of Motherhood” (MLM) can be understood as the overall mental load required to parent. MLM involves monitoring tasks that need to be completed while simultaneously managing the past, present, and future emotions of each family member individually, as well as the collective family (83). MLM encompasses a component of cognitive labor, emotional labor, and is thought to be impacted by psychosocial stressors (87). Beyond the hands-on tasks of caregiving, MLM entails the often invisible work of managing household responsibilities, such as accountability for the task outcomes, anticipating and planning for the family’s long-term needs, making decisions, and monitoring progress, which is mentally taxing yet often invisible to both cognitive laborers and their partners (88). A phenomenological analysis of seven focus groups interviews with mothers of young children further delineated the definition of a mothers’ mental labor, grounded in lived experience of mothers (90). The mental labor of motherhood emerged as a set of six cognitive activities aimed at accomplishing family goals: planning and strategizing, monitoring and anticipating needs, meta-parenting (thinking and reflection about parenting), knowing (learning and remembering), managerial thinking (including delegating and instructing), and self-regulation (90).

In addition to cognitive labor, within the mental load of motherhood also lies emotional labor, which is defined as the work of managing one’s own emotions and those of others. In the setting of family life, emotional labor is the work of anticipating, thinking, and caring about family needs and feelings (83). Emotion regulation and executive functioning are important skills in this work, as the there is a need to regulate one’s own emotions in order to respond to children with patience and sensitivity, and there is often a need to suppress one’s own thoughts and emotions to prioritize caregiving. Thus, emotional labor is a core component of MLM, requiring continuous emotional attunement and self-regulation in service of the family’s emotional well-being.

Psychosocial and structural factors play a critical role in the increased modern day mental load of motherhood. Firstly, despite improvements in domestic labor inequality, disparities remain in the division of domestic work. Mothers often bear the bulk of the physical household labor, with an even more disproportionate share of the cognitive load of household responsibilities (88, 89, 91). Social determinants of health further exacerbate modern stressors for subgroups of women facing additional adversities. Factors such as cultural values, minority stress, financial burden, parental leave policies, the isolation of nuclear family structures, the stress of single parenting, and other interpersonal and family dynamics contribute to MLM (87, 90). Emerging literature from neuroimaging studies of the maternal brain suggest potential interactive effects of these factors with cognitive load on maternal brain functioning, which may present a neurocognitive mediator of heightened risk for postpartum mental health problems. Evidence reviewed in Kim et al. (2021) demonstrates overall that a larger number of socioeconomic, physical, environmental, and psychosocial stressors is associated with altered maternal brain activation in areas important for emotional and cognitive empathy in response to infant cues, which in turn impacts a mother’s capacity for sensitive caregiving, decision-making, and emotion regulation (37, 87, 92). More optimistically, two separate interventions aimed at improving emotional regulation skills and inhibitory control among low income women have demonstrated effectiveness in improving parenting skills and maternal wellbeing, highlighting EF as a potential modifiable intervention target for at-risk groups (93, 94). Social policies can also have positive impacts: for example, policies supporting mothers through paid maternity leave are associated with reduced maternal stress and improved familial mental health (95). Still, further research is needed to determine which familial, institutional, and social factors surrounding modern day motherhood contribute most to the mental load burden, and how MLM interacts with broader social determinants of health.

Neuroscience has scarcely accounted for the mental load of motherhood. It remains an unmeasured but potentially significant factor in understanding perinatal cognitive and mood changes. Cognitive adaptations to parenting and managing MLM place demands on executive functioning include cognitive flexibility, emotional regulation, theory of mind, decision making, goal-directed behavior, and reward sensitivity (18, 61, 96). Executive functioning is core to daily functioning, well-being, the regulation of cognitive processes that impact the quality of life, as well as multiple aspects of childcare, including anticipating, identifying, scheduling, planning, organizing, deciding, and ultimately ensuring that household and childcare-related tasks occur.

It is unclear how MLM and EF intersect to contribute to mood and subjective cognition in the peripartum (41, 97). Existing research exploring the etiologies of pregnancy-related memory difficulties have attributed this to complex hormonal changes, changes in neurotransmitters, changes in the chronological age of circulating erythrocytes, mood alteration, cultural stereotypes, and lifestyle factors (41, 46, 49, 98100). The role of MLM in these subjective cognitive changes has not been well accounted for, though it is an important factor in maternal well-being. Cognitive labor has been linked to heightened risks of maternal depression, stress, burnout, and relationship strain (89). The cognitive load of parenting seems to be particularly taxing, as evidence suggests that sharing cognitive labor with a partner is more effective at reducing maternal stress than merely delegating physical tasks like diaper changing (101, 102). Thus, the growing burden of the mental load of motherhood is likely a key factor driving vulnerability to mental illness across matrescence (87). The complex phenomenon of the mental load of motherhood impacts the majority of mothers and must be measured and integrated into maternal mental health research (87).

4 Discussion

4.1 Summary of findings

The evidence reviewed highlights the strong association between MDD and executive function impairments, reinforcing cognitive theories that suggest these deficits contribute to the onset and maintenance of depression. The persistence of EF deficits even in remitted individuals underscores their relevance as both a state and trait marker of depression. Given the cognitive and emotional regulation demands of the perinatal period, such findings provide a valuable framework for understanding similar impairments in postpartum depression. The mental load of motherhood, coupled with neuroplastic changes in the perinatal brain, may further exacerbate EF vulnerabilities during this time and heighten risk for PMADs.

Although the literature on MDD and EF is extensive, evidence for EF changes in PPD remains more limited. Current findings suggest that PPD may also be associated with decrements in EF that are essential for managing the demands of parenting, including worse cognitive inhibition, working memory, and short-term memory (6365). These EF decrements may contribute to difficulties in caregiving, potentially increasing maternal stress and worsening mood symptoms. However, research on the relationship between PPD and executive function remains limited, with a predominance of cross-sectional studies.

Structural brain changes during matrescence more broadly, in frontal cortical regions that are strongly associated with executive functioning, reinforce a potential role of EF in both adaptation to parenting and vulnerability to mental illness. Despite the common experience of “mommy brain, “ existing research has shown that cognitive changes across the perinatal period are relatively subtle and primarily emerge during cognitive tasks that place high demand on executive function (27, 41, 43, 4749). Although a meta-analysis supports this finding, significant heterogeneity across studies and inconsistent results limit definitive conclusions.

4.2 Limitations and gaps in the literature

Until recently, there has been a striking lack of research on the maternal brain across the perinatal period. This gap reflects broader systemic issues in science, where women’s health research has historically been underfunded and overlooked, hindering progress in understanding and improving maternal mental health (103). Inconsistent findings across existing studies may stem from variability in cognitive tasks, timing of assessments, and the heterogeneity of perinatal populations. Longitudinal research, with more consistent methodologies such as cognitive tasks and time points, is essential for capturing the dynamic cognitive and emotional changes across the perinatal period, and for identifying early markers of risk. There is also growing recognition that pregnant women and mothers with PPD are not a homogenous group. A recent systematic review identified four major symptom trajectories within PPD, highlighting the need to move beyond static models of perinatal depression (104). Longitudinal designs, by studying the same people over time, are essential for distinguishing true cognitive shifts from individual variability.

Possible parallels between EF impairments in MDD and those reported in postpartum depression invites further investigation into whether cognitive difficulties during the perinatal period might reflect maladaptive changes associated with the onset of mood disorders versus expected neuroplastic and cognitive adaptations to the demands of motherhood. Cognitive resource allocation theory suggests that during the perinatal period, neural resources may be redistributed from executive function domains toward enhanced social-cognitive capacities, such as emotional processing and theory of mind, to enhance caregiving (105). This adaptive perspective challenges deficit-based perspectives and highlights the need for research that can differentiate between maladaptive impairment and adaptive reorganization supporting the transition to parenthood.

4.3 Future directions and recommendations

To advance understanding of EF changes across the perinatal period, several research priorities emerge. Longitudinal designs are needed to understand normative cognitive trajectories over time, better control for individual variability, and distinguish between transient shifts and lasting impairments. Future studies should also adopt ecologically valid assessments, including parenting-relevant stimuli and home-based cognitive tasks to better capture possible adaptive enhancements as well as the impact of the real-world cognitive demands of motherhood on EF and memory performance. Future research should also study maternal cognitive and mental health in context. The early postpartum time frame has a number of confounding physiological effects, including sleep deprivation, stress, fluctuating neurohormones, baby blues, parity, and the often overlooked emotional and cognitive labor of motherhood, all of which interact with cognitive function and mental health outcomes (106). There is a need to better understand how the cognitive and emotional labor of parenting might interact with neural plasticity, executive function, and ultimately risk of psychiatric illness.

Reconceptualizing “mommy brain” as a potential form of cognitive adaptation, rather than solely a deficit may help shift narratives and advance science, as cognitive resources during matrescence may not be diminished but reprioritized (107). A nuanced reconceptualization of “mommy brain” within the context of the modern-day mental load of motherhood and with respect to neural adaptations to parenting will integrate neurobiological perspectives and social determinants of health, ultimately advancing a more comprehensive approach to maternal mental health.

5 Conclusion

The perinatal period represents a time of profound neurobiological, cognitive, and emotional change. While these adaptations support the transition to motherhood, they also may heighten vulnerability to mental health challenges, including PPD. Executive function, as a critical cognitive domain, plays a central role in managing the mental load of motherhood and has also been implicated in depressive disorders. Understanding normative EF changes during this period is essential for better understanding the relationship between EF, perinatal depression, and the mental load of motherhood. Consideration for these cognitive, neurobiological, and psychosocial factors of matrescence is critical for addressing maternal mental health and developing interventions that support parental well-being.

Author contributions

TG: Conceptualization, Investigation, Writing – original draft, Writing – review & editing. CM: Conceptualization, Methodology, Supervision, Writing – review & editing.

Funding

The author(s) declare financial support was received for the research and/or publication of this article. Supported by a Brain Behavior Research Foundation Young Investigator award to CM.

Conflict of interest

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Generative AI statement

The author(s) declare that no Generative AI was used in the creation of this manuscript.

Any alternative text (alt text) provided alongside figures in this article has been generated by Frontiers with the support of artificial intelligence and reasonable efforts have been made to ensure accuracy, including review by the authors wherever possible. If you identify any issues, please contact us.

Publisher’s note

All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher.

References

1. Office of the Surgeon General. Parents under pressure: the U.S. Surgeon general's advisory on the mental health & Well-being of parents. Washington, DC: U.S. Public Health Services (2024).

Google Scholar

2. Office of the Surgeon General. The surgeon general’s call to action to improve maternal health. Washington, DC: U.S. Department of Health & Human Services (2024).

Google Scholar

3. Haight SC, Daw JR, Martin CL, Sheffield-Abdullah K, Verbiest S, Pence BW, et al. Racial and ethnic inequities in postpartum depressive symptoms, diagnosis, and care in 7 US jurisdictions. Health Affairs. (2024) 43:486–95 . doi: 10.1377/hlthaff.2023.01434

PubMed Abstract | Crossref Full Text | Google Scholar

4. Bauman BL, Ko JY, Cox S, D'Angelo Mph DV, Warner L, Folger S, et al. Vital signs: postpartum depressive symptoms and provider discussions about perinatal depression. United States CDC Morbidity Mortality Weekly Rep. (2020) 19:575–81. doi: 10.15585/mmwr.mm6919a2

PubMed Abstract | Crossref Full Text | Google Scholar

5. Carlson K, Mughal S, Azhar Y, and Siddiqui W. Perinatal depression. Treasure Island, FL: StatPearls (2025). Available online at: https://www.ncbi.nlm.nih.gov/books/NBK519070/ (Accessed February 10, 2025).

Google Scholar

6. Stein A, Pearson RM, Goodman SH, Rapa E, Rahman A, McCallum M, et al. Effects of perinatal mental disorders on the fetus and child. Lancet. (2014) 384:1800–19. doi: 10.1016/S0140-6736(14)61277-0

PubMed Abstract | Crossref Full Text | Google Scholar

7. Waxler E, Thelen K, and Muzik M. Maternal perinatal depression-impact on infant and child development. Eur Psychiatr Rev. (2011) 4:41–7.

Google Scholar

8. McKee K, Admon LK, Winkelman TNA, Muzik M, Hall S, Dalton VK, et al. Perinatal mood and anxiety disorders, serious mental illness, and delivery-related health outcomes, United States, 2006–2015. BMC Women's Health. (2020) 20. doi: 10.1186/s12905-020-00996-6

PubMed Abstract | Crossref Full Text | Google Scholar

9. Trost S, Beauregard J, Chandra G, Njie F, Harvey A, Berry J, et al. Pregnancy-related deaths: data from maternal mortality review committees in 36 US states, 2017-2019. Centers Dis Control Prevention US Department Health Hum Serv. (2022) 45.

Google Scholar

10. Athan AM. A critical need for the concept of matrescence in perinatal psychiatry. Front Psychiatry. (2024) 15:1364845. doi: 10.3389/fpsyt.2024.1364845

PubMed Abstract | Crossref Full Text | Google Scholar

11. Brunton PJ, Russell JA, Brunton PJ, and Russell JA. The expectant brain: adapting for motherhood. Nat Rev Neurosci. (2008) 9:11–25. doi: 10.1038/nrn2280

PubMed Abstract | Crossref Full Text | Google Scholar

12. Puri TA, Richard JE, and Galea LAM. Beyond sex differences: short- and long-term effects of pregnancy on the brain. Trends Neurosci. (2023) 46. doi: 10.1016/j.tins.2023.03.010

PubMed Abstract | Crossref Full Text | Google Scholar

13. Haim A, Julian D, Albin-Brooks C, Brothers HM, Lenz KM, Leuner B, et al. A survey of neuroimmune changes in pregnant and postpartum female rats. Brain Behavior Immun. (2017) 59. doi: 10.1016/j.bbi.2016.09.026

PubMed Abstract | Crossref Full Text | Google Scholar

14. Orchard ER, Rutherford HJV, Holmes AJ, and Jamadar SD. Matrescence: lifetime impact of motherhood on cognition and the brain. Trends Cogn Sci. (2023) 27. doi: 10.1016/j.tics.2022.12.002

PubMed Abstract | Crossref Full Text | Google Scholar

15. Feldman R. The adaptive human parental brain: implications for children's social development. Trends Neurosci. (2015) 38:387–99. doi: 10.1016/j.tins.2015.04.004

PubMed Abstract | Crossref Full Text | Google Scholar

16. Rosenblatt JS. Prepartum and postpartum regulation of maternal behaviour in the rat. Ciba Foundation symposium. (1975) 33:17–37. doi: 10.1002/9780470720158.ch3

PubMed Abstract | Crossref Full Text | Google Scholar

17. Kempermann G. Giving birth gives birth to neurons. Science. (2023) 382:881–2. doi: 10.1126/science.adl2399

PubMed Abstract | Crossref Full Text | Google Scholar

18. Hoekzema E, Barba-Müller E, Pozzobon C, Picado M, Lucco F, García-García D, et al. Pregnancy leads to long-lasting changes in human brain structure. Nat Neurosci. (2016) 20:287–96. doi: 10.1038/nn.4458

PubMed Abstract | Crossref Full Text | Google Scholar

19. Pritschet L, Taylor CM, Cossio D, Faskowitz J, Santander T, Handwerker DA, et al. Neuroanatomical changes observed over the course of a human pregnancy. Nat Neurosci. (2024) 27:2253–60. doi: 10.1038/s41593-024-01741-0

PubMed Abstract | Crossref Full Text | Google Scholar

20. Servin-Barthet C, Martínez-García M, Paternina-Die M, Marcos-Vidal L, Martín de Blas D, Soler A, et al. Pregnancy entails a U-shaped trajectory in human brain structure linked to hormones and maternal attachment. Nat Commun. (2025) 16:730. doi: 10.1038/s41467-025-55830-0

PubMed Abstract | Crossref Full Text | Google Scholar

21. McCormack C, Thomason M, McCormack C, and Thomason M. Pregnancy restructures the brain to prepare for childbirth and parenthood. Nature. (2024) 636:583–4. doi: 10.1038/d41586-024-03942-w

PubMed Abstract | Crossref Full Text | Google Scholar

22. Pawluski JL, Hoekzema E, Leuner B, and Lonstein JS. Less can be more: Fine tuning the maternal brain. Neurosci Biobehav Rev. (2022) 133:104475. doi: 10.1016/j.neubiorev.2021.11.045

PubMed Abstract | Crossref Full Text | Google Scholar

23. van 't Hof SR, Straathof M, Spalek K, and Hoekzema E. Theory of mind during pregnancy and postpartum: A systematic review. J Neuroendocrinol. (2023) 35. doi: 10.1111/jne.13266

PubMed Abstract | Crossref Full Text | Google Scholar

24. Martínez-García M, Jacobs EG, de Lange AMG, and Carmona S. Advancing the neuroscience of human pregnancy. Nat Neurosci. (2024) 27:805–7. doi: 10.1038/s41593-024-01629-z

PubMed Abstract | Crossref Full Text | Google Scholar

25. Heller C, Barth C, Silk TJ, Vijayakumar N, Carmona S, Martínez-García M, et al. The ENIGMA-Neuroendocrinology working group to bridge gaps in female mental health research. Nat Ment Health. (2024) 2:348–50. doi: 10.1038/s44220-024-00224-2

Crossref Full Text | Google Scholar

26. Pessoa L and Pessoa L. On the relationship between emotion and cognition. Nat Rev Neurosci. (2008) 9:148–58. doi: 10.1038/nrn2317

PubMed Abstract | Crossref Full Text | Google Scholar

27. Davies SJ, Lum JA, Skouteris H, Byrne LK, and Hayden MJ. Cognitive impairment during pregnancy: a meta-analysis. Med J Aust. (2018) 208:35–40. doi: 10.5694/mja17.00131

PubMed Abstract | Crossref Full Text | Google Scholar

28. Diamond A and Diamond A. Executive functions. Annu Rev Psychol. (2013) 64:135–68. doi: 10.1146/annurev-psych-113011-143750

PubMed Abstract | Crossref Full Text | Google Scholar

29. Johnson SL, Elliott MV, and Carver CS. Impulsive responses to positive and negative emotions: parallel neurocognitive correlates and their implications. Biol Psychiatry. (2020) 87:338–49. doi: 10.1016/j.biopsych.2019.08.018

PubMed Abstract | Crossref Full Text | Google Scholar

30. Bartholomew ME, Heller W, and Miller GA. Inhibitory control of emotional processing: Theoretical and empirical considerations. Int J Psychophysiol. (2021) 163:5–10. doi: 10.1016/j.ijpsycho.2019.03.015

PubMed Abstract | Crossref Full Text | Google Scholar

31. Miola A, Cattarinussi G, Antiga G, Caiolo S, Solmi M, Sambataro F, et al. Difficulties in emotion regulation in bipolar disorder: A systematic review and meta-analysis. J Affect Disord. (2022) 302:352–60. doi: 10.1016/j.jad.2022.01.102

PubMed Abstract | Crossref Full Text | Google Scholar

32. Aldao A, Nolen-Hoeksema S, and Schweizer S. Emotion-regulation strategies across psychopathology: A meta-analytic review. Clin Psychol Rev. (2010) 30:217–37. doi: 10.1016/j.cpr.2009.11.004

PubMed Abstract | Crossref Full Text | Google Scholar

33. Kraiss JT, Ten Klooster PM, Moskowitz JT, and Bohlmeijer ET. The relationship between emotion regulation and well-being in patients with mental disorders: A meta-analysis. Compr Psychiatry. (2020) 102:152189. doi: 10.1016/j.comppsych.2020.152189

PubMed Abstract | Crossref Full Text | Google Scholar

34. Rutherford HJV, Wallace NS, Laurent HK, and Mayes LC. Emotion regulation in parenthood. Dev Rev. (2015) 36:1–14. doi: 10.1016/j.dr.2014.12.008

PubMed Abstract | Crossref Full Text | Google Scholar

35. Crandall A, Deater-Deckard K, and Riley AW. Maternal emotion and cognitive control capacities and parenting: A conceptual framework. Dev Rev. (2015) 36:105–26. doi: 10.1016/j.dr.2015.01.004

PubMed Abstract | Crossref Full Text | Google Scholar

36. Parental emotion and emotion regulation: A critical target of study for research and intervention to promote child emotion socialization. Dev Psychol. (2020) 56:408. doi: 10.1037/dev0000864

PubMed Abstract | Crossref Full Text | Google Scholar

37. Hajal NJ and Paley B. How stress can influence brain adaptations to motherhood. Front Neuroendocrinol. (2021) 60. doi: 10.1016/j.yfrne.2020.100875

PubMed Abstract | Crossref Full Text | Google Scholar

38. Silk JS, Shaw DS, Skuban EM, Oland AA, and Kovacs M. Journal of Child Psychology and Psychiatry. J Child Psychol Psychiatry. (2006) 47:69–78. doi: 10.1111/j.1469-7610.2005.01440.x

PubMed Abstract | Crossref Full Text | Google Scholar

39. Bariola E, Hughes EK, and Gullone E. Relationships between parent and child emotion regulation strategy use: A brief report. J Child Family Stud. (2011) 21:443–8. doi: 10.1007/s10826-011-9497-5

Crossref Full Text | Google Scholar

40. Maternal and adolescent distress tolerance: The moderating role of gender. Emotion. (2014) 14:416. doi: 10.1037/a0034991

PubMed Abstract | Crossref Full Text | Google Scholar

41. Daughters SB, Gorka SM, Rutherford HJV, and Mayes LC. Cognitive changes in pregnancy: mild decline or societal stereotype? Appl Cogn Psychol. (2008) 22:1142–62. doi: 10.1002/acp.1427

Crossref Full Text | Google Scholar

42. Ouellette SJ and Hampson E. Memory and affective changes during the antepartum: A narrative review and integrative hypothesis. J Clin Exp Neuropsychol. (2019) 41:87–107. doi: 10.1080/13803395.2018.1485881

PubMed Abstract | Crossref Full Text | Google Scholar

43. Logan DM, Hill KR, Jones R, Holt-Lunstad J, and Larson MJ. How do memory and attention change with pregnancy and childbirth? A controlled longitudinal examination of neuropsychological functioning in pregnant and postpartum women. J Clin Exp Neuropsychol. (2014) 36:528–39. doi: 10.1080/13803395.2014.912614

PubMed Abstract | Crossref Full Text | Google Scholar

44. Stevanovic D. Quality of Life Enjoyment and Satisfaction Questionnaire – short form for quality of life assessments in clinical practice: a psychometric study. J Psychiatr Ment Health Nurs. (2011) 18:744–50. doi: 10.1111/j.1365-2850.2011.01735.x

PubMed Abstract | Crossref Full Text | Google Scholar

45. Janes C, Casey P, Huntsdale C, and Angus G. Memory in pregnancy. I: Subjective experiences and objective assessment of implicit, explicit and working memory in primigravid and primiparous women. J Psychosomatic Obstetrics Gynecology. (1999) 20:80–7. doi: 10.3109/01674829909075580

PubMed Abstract | Crossref Full Text | Google Scholar

46. Brett M and Baxendale S. Motherhood and memory: a review. Psychoneuroendocrinology. (2001) 26:339–62. doi: 10.1016/S0306-4530(01)00003-8

PubMed Abstract | Crossref Full Text | Google Scholar

47. Farrar D, Tuffnell D, Neill J, Scally A, and Marshall K. Assessment of cognitive function across pregnancy using CANTAB: A longitudinal study. Brain Cogn. (2014) 84:76–84. doi: 10.1016/j.bandc.2013.11.003

PubMed Abstract | Crossref Full Text | Google Scholar

48. Casey P and Casey P. A longitudinal study of cognitive performance during pregnancy and new motherhood. Arch Women's Ment Health. (2000) 3:65–76. doi: 10.1007/s007370070008

Crossref Full Text | Google Scholar

49. Henry JD and Rendell PG. A review of the impact of pregnancy on memory function. J Clin Exp Neuropsychol. (2007) 29:793–803. doi: 10.1080/13803390701612209

PubMed Abstract | Crossref Full Text | Google Scholar

50. Jensen AR and Rohwer WD. The stroop color-word test: A review. Acta Psychologica. (1966) 25:36–93. doi: 10.1016/0001-6918(66)90004-7

PubMed Abstract | Crossref Full Text | Google Scholar

51. Hilbert S, Nakagawa TT, Puci P, Zech A, and Bühner M. The digit span backwards task. Eur J psychol Assess. (2014) 31. doi: 10.1027/1015-5759/a000223

Crossref Full Text | Google Scholar

52. Kaufman AS and Kaufman AS. Test review: wechsler, D. Manual for the wechsler adult intelligence scale, revised. New york: psychological corporation, 1981. J Psychoeducational Assess. (1983) 1:309–13. doi: 10.1177/073428298300100310

Crossref Full Text | Google Scholar

53. Kumari S, Koppad R, Singh A, Singh B, Qazi MS, Jaber Amin MH, et al. Prevalence of cognitive dysfunction and associated behavioral changes, lactational failure, and their determinants among postpartum women in South India: A community-based study. Int J gynaecology obstetrics: Off Organ Int Fed Gynaecology Obstetrics. (2025) 170. doi: 10.1002/ijgo.70062

PubMed Abstract | Crossref Full Text | Google Scholar

54. Zheng JX, Ge L, Chen H, Yin X, Chen YC, Tang WW, et al. Disruption within brain default mode network in postpartum women without depression. Medicine. (2020) 99:20045. doi: 10.1097/MD.0000000000020045

PubMed Abstract | Crossref Full Text | Google Scholar

55. Everyday life memory deficits in pregnant women. Can J Exp Psychol. (2011) 65:27. doi: 10.1037/a0022844

PubMed Abstract | Crossref Full Text | Google Scholar

56. Cuttler C, Graf P, Pawluski JL, and Galea LAM. Mommy brain in the United States. Ethos. (2023) 51:111–29. doi: 10.1111/etho.12381

Crossref Full Text | Google Scholar

57. American Psychiatric Association. Diagnostic and statistical manual of mental disorders. Arlington, VA: American Psychiatric Assocaition (2013). doi: 10.1176/appi.books.9780890425596.

Crossref Full Text | Google Scholar

58. O'Hara MW, McCabe JE, O'Hara MW, and McCabe JE. Postpartum depression: current status and future directions. Annu Rev Clin Psychol. (2013) 9:379–407. doi: 10.1146/annurev-clinpsy-050212-185612

PubMed Abstract | Crossref Full Text | Google Scholar

59. Levin G, Ein-Dor T, Levin G, and Ein-Dor T. A unified model of the biology of peripartum depression. Trans Psychiatry. (2023) 13:138. doi: 10.1038/s41398-023-02439-w

PubMed Abstract | Crossref Full Text | Google Scholar

60. Swain JE, Lorberbaum JP, Kose S, and Strathearn L. Brain basis of early parent–infant interactions: psychology, physiology, and in vivo functional neuroimaging studies. J Child Psychol Psychiatry. (2007) 48:262–87. doi: 10.1111/j.1469-7610.2007.01731.x

PubMed Abstract | Crossref Full Text | Google Scholar

61. Pawluski JL. The parental brain, perinatal mental illness, and treatment: A review of key structural and functional changes. Semin perinatology. (2024) 48:151951. doi: 10.1016/j.semperi.2024.151951

PubMed Abstract | Crossref Full Text | Google Scholar

62. Pawluski JL, Lonstein JS, and Fleming AS. The neurobiology of postpartum anxiety and depression. Trends Neurosci. (2017) 40:106–20. doi: 10.1016/j.tins.2016.11.009

PubMed Abstract | Crossref Full Text | Google Scholar

63. Pio de Almeida LS, Jansen K, Köhler CA, Pinheiro RT, da Silva RA, Bonini JS, et al. Working and short-term memories are impaired in postpartum depression. J Affect Disord. (2012) 136:1238–42. doi: 10.1016/j.jad.2011.09.031

PubMed Abstract | Crossref Full Text | Google Scholar

64. Kataja EL, Karlsson L, Huizink AC, Tolvanen M, Parsons C, Nolvi S, et al. Pregnancy-related anxiety and depressive symptoms are associated with visuospatial working memory errors during pregnancy. J Affect Disord. (2017) 218:66–74. doi: 10.1016/j.jad.2017.04.033

PubMed Abstract | Crossref Full Text | Google Scholar

65. Bao C, Wang Y, Le T, Xu L, Tang W, Zou W, et al. Relationship between depressive symptoms and sleep quality and cognitive inhibition ability in prenatal pregnant women. BMC Psychiatry. (2023) 23:522. doi: 10.1186/s12888-023-04976-6

PubMed Abstract | Crossref Full Text | Google Scholar

66. Bora E, Yucel M, and Pantelis C. Cognitive endophenotypes of bipolar disorder: A meta-analysis of neuropsychological deficits in euthymic patients and their first-degree relatives. J Affect Disord. (2009) 113. doi: 10.1016/j.jad.2008.06.009

PubMed Abstract | Crossref Full Text | Google Scholar

67. Hasler G, Drevets WC, Manji HK, and Charney DS. Discovering endophenotypes for major depression. Neuropsychopharmacology. (2004) 29:1765–81. doi: 10.1038/sj.npp.1300506

PubMed Abstract | Crossref Full Text | Google Scholar

68. LeMoult J and Gotlib IH. Depression: A cognitive perspective. Clin Psychol Rev. (2019) 69. doi: 10.1016/j.cpr.2018.06.008

PubMed Abstract | Crossref Full Text | Google Scholar

69. Roiser JP, Elliott R, and Sahakian BJ. Cognitive mechanisms of treatment in depression. Neuropsychopharmacology. (2011) 37:117–36. doi: 10.1038/npp.2011.183

PubMed Abstract | Crossref Full Text | Google Scholar

70. Harvey PO, Fossati P, Pochon JB, Levy R, Lebastard G, Lehéricy S, et al. Cognitive control and brain resources in major depression: an fMRI study using the n-back task. NeuroImage. (2005) 26:860–9. doi: 10.1016/j.neuroimage.2005.02.048

PubMed Abstract | Crossref Full Text | Google Scholar

71. Korgaonkar MS, Grieve SM, Etkin A, Koslow SH, and Williams LM. Using standardized fMRI protocols to identify patterns of prefrontal circuit dysregulation that are common and specific to cognitive and emotional tasks in major depressive disorder: first wave results from the iSPOT-D study. Neuropsychopharmacology: Off Publ Am Coll Neuropsychopharmacol. (2013) 38:863–71. doi: 10.1038/npp.2012.252

PubMed Abstract | Crossref Full Text | Google Scholar

72. Li X-Y, Chen X, and Yan C-G. Altered cerebral activities and functional connectivity in depression: a systematic review of fMRI studies. Quantitative Biol. (2022) 10:366–80. doi: 10.15302/J-QB-021-0270

Crossref Full Text | Google Scholar

73. Kriesche D, Woll CFJ, Tschentscher N, Engel RR, and Karch S. Neurocognitive deficits in depression: a systematic review of cognitive impairment in the acute and remitted state. Eur Arch Psychiatry Clin Neurosci. (2022) 273:1105–28. doi: 10.1007/s00406-022-01479-5

PubMed Abstract | Crossref Full Text | Google Scholar

74. Synder HR. Major depressive disorder is associated with broad impairments on neuropsychological measures of executive function: a meta-analysis and review. psychol Bull. (2013) 139:81. doi: 10.1037/a0028727

PubMed Abstract | Crossref Full Text | Google Scholar

75. Nuño L, Gómez-Benito J, Carmona VR, and Pino O. A systematic review of executive function and information processing speed in major depression disorder. Brain Sci. (2021) 11:147. doi: 10.3390/brainsci11020147

PubMed Abstract | Crossref Full Text | Google Scholar

76. Afridi MI, Hina M, Qureshi IS, and Hussain M. Cognitive disturbance comparison among drug-naïve depressed cases and healthy controls. J Coll Physicians Surg Pak. (2011) 21:351–5.

PubMed Abstract | Google Scholar

77. Rock PL, Roiser JP, Riedel WJ, and Blackwell AD. Cognitive impairment in depression: a systematic review and meta-analysis. psychol Med. (2014) 44:2029–40. doi: 10.1017/S0033291713002535

PubMed Abstract | Crossref Full Text | Google Scholar

78. Bhalla RK, Butters M, Mulsant BH, Begley AE, Zmuda M, Schoderbek B, et al. Persistence of neuropsychologic deficits in the remitted state of late-life depression. Am J Geriatric Psychiatry. (2006) 14:419–27. doi: 10.1097/01.JGP.0000203130.45421.69

PubMed Abstract | Crossref Full Text | Google Scholar

79. Reppermund S, Ising M, Lucae S, and Zihl J. Cognitive impairment in unipolar depression is persistent and non-specific: further evidence for the final common pathway disorder hypothesis. psychol Med. (2009) 39:603–14. doi: 10.1017/S003329170800411X

PubMed Abstract | Crossref Full Text | Google Scholar

80. Potter GG, Kittinger JD, Wagner HR, Steffens DC, and Krishnan RRR. Prefrontal neuropsychological predictors of treatment remission in late-life depression. Neuropsychopharmacology. (2004) 29:2266–71. doi: 10.1038/sj.npp.1300551

PubMed Abstract | Crossref Full Text | Google Scholar

81. Halahakoon DC, Lewis G, and Roiser JP. Cognitive impairment and depression—Cause, consequence, or coincidence? JAMA Psychiatry. (2019) 76:239–40. doi: 10.1001/jamapsychiatry.2018.3631

PubMed Abstract | Crossref Full Text | Google Scholar

82. Gaillard AWK. Comparing the concepts of mental load and stress. Ergonomics. (1993) 36:991–1005. doi: 10.1080/00140139308967972

PubMed Abstract | Crossref Full Text | Google Scholar

83. Dean L, Churchill B, and Ruppanner L. The mental load: building a deeper theoretical understanding of how cognitive and emotional labor overload women and mothers. Community Work Family. (2022) 25:13–29. doi: 10.1080/13668803.2021.2002813

Crossref Full Text | Google Scholar

84. Díaz-García J, González-Ponce I, Ponce-Bordón JC, López-Gajardo MÁ, Ramírez-Bravo I, Rubio-Morales A, et al. Mental load and fatigue assessment instruments: A systematic review. Int J Environ Res Public Health. (2022) 19:419. doi: 10.3390/ijerph19010419

PubMed Abstract | Crossref Full Text | Google Scholar

85. Sanders AF. Some remarks on mental load. Ment Workload. (1979) 41–7. doi: 10.1007/978-1-4757-0884-4_5

Crossref Full Text | Google Scholar

86. Jiang H, Mizobuchi S, and Chignell M. Lower executive function ability may lead to higher perceived mental workload in driving scenarios. Proc Hum Factors Ergonomics Soc Annu Meeting. (2023) 67:747–54. doi: 10.1177/21695067231192859

Crossref Full Text | Google Scholar

87. Callaghan BL, McCormack C, Kim P, and Pawluski JL. Understanding the maternal brain in the context of the mental load of motherhood. Nat Ment Health. (2024) 2:764–72. doi: 10.1038/s44220-024-00268-4

Crossref Full Text | Google Scholar

88. Daminger A and Daminger A. The cognitive dimension of household labor. Am Sociological Rev. (2019) 84:609–33. doi: 10.1177/0003122419859007

Crossref Full Text | Google Scholar

89. Aviv E, Waizman Y, Kim E, Liu J, Rodsky E, Saxbe D, et al. Cognitive household labor: gender disparities and consequences for maternal mental health and wellbeing. Arch Women's Ment Health. (2024) 28:5–14. doi: 10.1007/s00737-024-01490-w

PubMed Abstract | Crossref Full Text | Google Scholar

90. Robertson LG, Anderson TL, Hall MEL, and Kim CL. Mothers and mental labor: A phenomenological focus group study of family-related thinking work. Psychol Women Q. (2019) 43:184–200. doi: 10.1177/0361684319825581

Crossref Full Text | Google Scholar

91. Lee Y-S and Waite LJ. Husbands’ and wives’ time spent on housework: A comparison of measures. J Marriage Family NCFR Family Sci J. (2005) 67:328–36. doi: 10.1111/j.0022-2445.2005.00119.x

Crossref Full Text | Google Scholar

92. Kim P, Capistrano C, and Congleton C. Socioeconomic disadvantages and neural sensitivity to infant cry: role of maternal distress. Soc Cogn Affect Neurosci. (2016) 11:1597–1607. doi: 10.1093/scan/nsw063

PubMed Abstract | Crossref Full Text | Google Scholar

93. Giuliani NR, Beauchamp KG, Noll LK, and Fisher PA. A preliminary study investigating maternal neurocognitive mechanisms underlying a child-supportive parenting intervention. Front Behav Neurosci. (2019) 13:16. doi: 10.3389/fnbeh.2019.00016

PubMed Abstract | Crossref Full Text | Google Scholar

94. Muzik M, Rosenblum KL, Alfafara EA, Schuster MM, Miller NM, Waddell RM, et al. Mom Power: preliminary outcomes of a group intervention to improve mental health and parenting among high-risk mothers. Arch Women's Ment Health. (2015) 18:507–21. doi: 10.1007/s00737-014-0490-z

PubMed Abstract | Crossref Full Text | Google Scholar

95. Jou J, Kozhimannil KB, Abraham JM, Blewett LA, and McGovern PM. Paid maternity leave in the United States: associations with maternal and infant health. Maternal Child Health J. (2017) 22:216–25. doi: 10.1007/s10995-017-2393-x

PubMed Abstract | Crossref Full Text | Google Scholar

96. Lambert KG. The parental brain: Transformations and adaptations. Physiol Behav. (2012) 107:792–800. doi: 10.1016/j.physbeh.2012.03.018

PubMed Abstract | Crossref Full Text | Google Scholar

97. Accortt EE and Wong MS. It is time for routine screening for perinatal mood and anxiety disorders in obstetrics and gynecology settings. Obstetrical Gynecological Survey. (2017) 72:553–68. doi: 10.1097/OGX.0000000000000477

PubMed Abstract | Crossref Full Text | Google Scholar

98. Shetty DN and Pathak SS. Correlation between plasma neurotransmitters and memory loss in pregnancy. J Reprod Med. (2002) 47:494–6.

PubMed Abstract | Google Scholar

99. Lunre S, Gidron Y, Piper I, Ben-Aroya Z, Sadan O, Boaz M, et al. Memory performance in late pregnancy and erythrocyte indices. J Soc Gynecologic Invest. (2005) 12:293–6. doi: 10.1016/j.jsgi.2005.01.001

PubMed Abstract | Crossref Full Text | Google Scholar

100. Harris ND, Deary IJ, Harris MB, Lees MM, and Wilson JA. Peripartal cognitive impairment: Secondary to depression? Br J Health Psychol. (1996) 1:127–36. doi: 10.1111/j.2044-8287.1996.tb00497.x

Crossref Full Text | Google Scholar

101. Thorstad RR, Anderson TL, Hall MEL, Willingham M, and Carruthers L. Breaking the mold. J Family Issues. (2006) 27:229–51. doi: 10.1177/0192513X05282189

Crossref Full Text | Google Scholar

102. Walzer S. Thinking about the baby: Gender and transitions into parenthood. Philadelphia, PA: Temple University Press (1998).

Google Scholar

103. Galea LA and Parekh RS. Ending the neglect of women’s health in research. BMJ. (2023) 381. doi: 10.1136/bmj.p1303

PubMed Abstract | Crossref Full Text | Google Scholar

104. Vanwetswinkel F, Bruffaerts R, Arif U, and Hompes T. The longitudinal course of depressive symptoms during the perinatal period: A systematic review. J Affect Disord. (2022) 315:213–23. doi: 10.1016/j.jad.2022.06.087

PubMed Abstract | Crossref Full Text | Google Scholar

105. Anderson MV and Rutherford MD. Cognitive reorganization during pregnancy and the postpartum period: an evolutionary perspective. Evolutionary Psychol. (2012) 10:659–87. doi: 10.1177/147470491201000402

PubMed Abstract | Crossref Full Text | Google Scholar

106. Chechko N, Losse E, Frodl T, and Nehls S. Baby blues, premenstrual syndrome and postpartum affective disorders: intersection of risk factors and reciprocal influences. BJPsych Open. (2024) 10:3. doi: 10.1192/bjo.2023.612

PubMed Abstract | Crossref Full Text | Google Scholar

107. McCormack C, Callaghan BL, and Pawluski JL. It’s time to rebrand “Mommy brain. JAMA Neurol. (2023) 80:335–6. doi: 10.1001/jamaneurol.2022.5180

PubMed Abstract | Crossref Full Text | Google Scholar

Keywords: pregnancy, cognition, executive function, maternal depression, mental load

Citation: Ghadimi TR and McCormack C (2025) Executive functioning in matrescence and implications for perinatal depression. Front. Psychiatry 16:1663017. doi: 10.3389/fpsyt.2025.1663017

Received: 10 July 2025; Accepted: 04 September 2025;
Published: 19 September 2025.

Edited by:

Laura Orsolini, Marche Polytechnic University, Italy

Reviewed by:

Chonnakarn Jatchavala, Prince of Songkla University, Thailand
Rosa Volgare, Marche Polytechnic University, Italy

Copyright © 2025 Ghadimi and McCormack. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

*Correspondence: T. Roxana Ghadimi, dHJnaGFkaW1pQGdtYWlsLmNvbQ==; Clare McCormack, Y2xhcmUubWNjb3JtYWNrQG55dWxhbmdvbmUub3Jn

Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.