Bachelor of Arts, Adelphi University (2014)
Master of Arts, CUNY Queens College (2016)
Doctor of Philosophy, CUNY Graduate School and University Center (2021)
Biological sensitivity to adolescent-parent discrepancies in perceived parental warmth.
2023; 16: 100211
Parenting behaviors are formative to the psychological development of young people; however, parent and adolescent perceptions of parenting are only moderately correlated with each other. Whereas discrepant perceptions may represent a normative process of deindividuation from caregivers in some adolescents, in others a discrepancy might predict psychological maladjustment. The biological sensitivity to context model provides a framework from which individual differences in development can be estimated in adolescents whose perceptions of parenting diverge from those of their parents.At baseline we obtained diurnal cortisol samples from US adolescents (M = 13.37 years of age, SD = 1.06) as well as parents' and adolescents' ratings of parental warmth; we obtained adolescent-reported symptoms of psychopathology at baseline and again at follow-up two years later (N = 108, 57.5% female). We estimated waking cortisol, cortisol awakening response, and daytime cortisol slopes using piecewise regression models.Lower adolescent than parent ratings of parental warmth predicted increased externalizing symptoms at follow-up. Higher waking cortisol and steeper cortisol awakening response and daytime slopes predicted increased internalizing symptoms at follow-up. Further, discrepant ratings of parental warmth interacted with cortisol awakening response and daytime slopes such that greater discrepancies predicted greater increases in externalizing symptoms in adolescents with steeper cortisol slopes.These findings indicate that steeper changes in cortisol production throughout the day index a greater sensitivity to perceived parental warmth. Lower adolescent than parent ratings of parental warmth may represent dysfunction in the parental relationship rather than a normative process of deindividuation in adolescents with steeper diurnal cortisol slopes.
View details for DOI 10.1016/j.cpnec.2023.100211
View details for PubMedID 37808874
View details for PubMedCentralID PMC10550797
Early life stress, sleep disturbances, and depressive symptoms during adolescence: The role of the cingulum bundle.
Developmental cognitive neuroscience
2023; 63: 101303
Adolescence is often characterized by sleep disturbances that can affect the development of white matter tracts implicated in affective and cognitive regulation, including the cingulate portion of the cingulum bundle (CGC) and the uncinate fasciculus (UF). These effects may be exacerbated in adolescents exposed to early life adversity (ELA). We examined the longitudinal relations between sleep problems and CGC and UF microstructure during adolescence and their relation to depressive symptoms as a function of exposure to ELA. We assessed self-reported sleep disturbances and depressive symptoms and acquired diffusion-weighted MRI scans twice: in early adolescence (9-13 years) and four years later (13-17 years) (N=72 complete cases). Independent of ELA, higher initial levels and increases in sleep problems were related to increases in depressive symptoms. Further, increases in right CGC fractional anisotropy (FA) mediated the association between sleep problems and depressive symptoms for youth who experienced lower, but not higher, levels of ELA. In youth with higher ELA, higher initial levels of and steeper decreases in sleep problems were associated with greater decreases in right UF FA, but were unrelated to depressive symptoms. Our findings highlight the importance of sleep quality in shaping fronto-cingulate-limbic tract development and depressive symptoms during adolescence.
View details for DOI 10.1016/j.dcn.2023.101303
View details for PubMedID 37738837
Maternal-prenatal stress and depression predict infant temperament during the COVID-19 pandemic.
Development and psychopathology
Researchers have begun to examine the psychological toll of the ongoing global COVID-19 pandemic. Data are now emerging indicating that there may be long-term adverse effects of the pandemic on new mothers and on children born during this period. In a longitudinal study of maternal mental health and child emotional development during the pandemic, we conducted online assessments of a cohort of women at two time points: when they were pregnant at the beginning of the surge of the pandemic in the United States (baseline, N = 725), and approximately 1 year postpartum (follow-up, N = 296), examining prenatal and postnatal maternal mental health, prenatal pandemic-related stress, and infant temperament. Pandemic-related stress at baseline was associated with concurrent depressive symptoms and infant negative affect at follow-up. Baseline maternal depressive symptoms were associated with follow-up depressive symptoms, which in turn were also associated with infant negative affect. Pandemic-related stress during pregnancy may have enduring effects on infant temperament. These findings have important implications for our understanding of the emotional development of children who were in utero during the COVID-19 pandemic.
View details for DOI 10.1017/S0954579422001055
View details for PubMedID 36345652
Negative caregiving and stress reactivity moderate the relation between early life stress and externalizing in adolescence.
2022; 64 (7): e22327
Exposure to early life stress (ELS) is common and has been implicated in the development of psychopathology; importantly, however, many individuals who experience ELS do not develop emotional or behavioral difficulties. Prior research implicates stress exposure, negative caregiving behaviors, and patterns of physiological reactivity in predicting psychological well-being; however, the precise factors that contribute to resilience versus vulnerability to the adverse effects of stress exposures are not well understood. In a longitudinal study of adolescents (N = 120) assessed at three timepoints approximately every 2 years beginning at the ages of 913 years, we examined the roles of autonomic reactivity to social stress (assessed through skin conductance during the Trier Social Stress Task) and negative caregiving behaviors as moderators of the association between exposure to ELS and internalizing and externalizing symptoms. We found that the relation between ELS and externalizing symptoms was moderated by both negative caregiving and autonomic reactivity, such that the relation between ELS and externalizing was positive at low levels of negative caregiving and at high levels of autonomic reactivity; interactions predicting internalizing symptoms were not statistically significant. These findings highlight the importance of considering physiological and environmental variables that might contribute to susceptibility or resilience to symptoms of psychopathology following exposure to ELS.
View details for DOI 10.1002/dev.22327
View details for PubMedID 36282754
View details for PubMedCentralID PMC9608333
A Social Gradient of Cortical Thickness in Adolescence: Relationships With Neighborhood Socioeconomic Disadvantage, Family Socioeconomic Status, and Depressive Symptoms.
Biological psychiatry global open science
2022; 2 (3): 253-262
BACKGROUND: Mental and physical health are affected by family and neighborhood socioeconomic status (SES). Accelerated maturation in the context of lower SES is one mechanism that might contribute to underlying health disparities; few studies, however, have considered neighborhood SES in relation to putative markers of brain maturation in adolescents.METHODS: In 120 adolescents 13 to 18 years of age, we examined family and neighborhood SES in relation to cortical thickness adjusted for age. We also examined whether cortical thickness was related to depressive symptoms and explored regions of interest.RESULTS: Controlling for age, neighborhood socioeconomic disadvantage was associated with a thinner cortex in the left hemisphere (standardized beta = -0.20), which was related to more severe depressive symptoms (standardized beta = -0.33). Family SES was not significantly associated with age-adjusted mean cortical thickness in either hemisphere after controlling for relevant covariates. In exploratory, covariate-adjusted analyses of cortical thickness at the regional level, neighborhood socioeconomic disadvantage was associated with reduced cortical thickness in the left superior frontal gyrus (standardized beta = -0.27), fusiform gyrus (standardized beta = -0.20), and insula (standardized beta = -0.21), whereas family SES was positively associated with cortical thickness in the right lateral and right medial orbitofrontal cortex (standardized beta = 0.21 and standardized beta = 0.19, respectively) and left transverse temporal gyrus (standardized beta = 0.22).CONCLUSIONS: Our findings provide evidence for a social gradient of cortical thickness during adolescence. Adolescents living in less advantaged community or family contexts appear to have a thinner cortex according to global and regional measures. Reduced cortical thickness in the left hemisphere may indicate increased risk for depression in adolescence.
View details for DOI 10.1016/j.bpsgos.2022.03.005
View details for PubMedID 36032055
Hippocampal volume indexes neurobiological sensitivity to the effect of pollution burden on telomere length in adolescents.
New directions for child and adolescent development
Exposure to environmental pollutants has been associated with cellular aging in children and adolescents. Individuals may vary, however, in their sensitivity or vulnerability to the effects of environmental pollutants. Larger hippocampal volume has emerged as a potential index of increased sensitivity to social contexts. In exploratory analyses (N=214), we extend work in this area by providing evidence that larger hippocampal volume in early adolescence reflects increased sensitivity to the effect of neighborhood pollution burden on telomere length (standardized beta =-0.40, 95% CI[-0.65, -0.15]). In contrast, smaller hippocampal volume appears to buffer this association (standardized beta =0.02). In youth with larger hippocampal volume, pollution burden was indirectly associated with shorter telomere length approximately 2 years later through shorter telomere length at baseline (indirect standardized beta =-0.25, 95% CI[-0.40, 0.10]). For these youth, living in high or low pollution-burdened neighborhoods may predispose them to develop shorter or longer telomeres, respectively, later in adolescence.
View details for DOI 10.1002/cad.20471
View details for PubMedID 35738556
Coping During the COVID-19 Pandemic: Maternal Mental Health and Infant Temperament
ELSEVIER SCIENCE INC. 2022: S196-S197
View details for Web of Science ID 000789022200480
Dimensions of Early Adversity and the Development of Functional Brain Network Connectivity During Adolescence: Implications for Trajectories of Internalizing Symptoms
ELSEVIER SCIENCE INC. 2022: S48
View details for Web of Science ID 000789022200122
Prenatal COVID-19 Related Stress, Maternal Emotion Regulation and Infant Temperament: Assessing the Developmental Impact of the COVID-19 Pandemic
ELSEVIER SCIENCE INC. 2022: S253
View details for Web of Science ID 000789022200620
An exploration of dimensions of early adversity and the development of functional brain network connectivity during adolescence: Implications for trajectories of internalizing symptoms.
Development and psychopathology
Different dimensions of adversity may affect mental health through distinct neurobiological mechanisms, though current supporting evidence consists largely of cross-sectional associations between threat or deprivation and fronto-limbic circuitry. In this exploratory three-wave longitudinal study spanning ages 9-19 years, we examined the associations between experiences of unpredictability, threat, and deprivation with the development of functional connectivity within and between three brain networks implicated in psychopathology: the salience (SAL), default mode (DMN), and fronto-parietal (FPN) networks, and tested whether network trajectories moderated associations between adversity and changes in internalizing symptoms. Connectivity decreased with age on average; these changes differed by dimension of adversity. Whereas family-level deprivation was associated with lower initial levels and more stability across most networks, unpredictability was associated with stability only in SAL connectivity, and threat was associated with stability in FPN and DMN-SAL connectivity. In youth exposed to higher levels of any adversity, lower initial levels and more stability in connectivity were related to smaller increases in internalizing symptoms. Our findings suggest that whereas deprivation is associated with widespread neurodevelopmental differences in cognitive and emotion processing networks, unpredictability is related selectively to salience detection circuitry. Studies with wider developmental windows should examine whether these neurodevelopmental alterations are adaptive or serve to maintain internalizing symptoms.
View details for DOI 10.1017/S0954579421001814
View details for PubMedID 35094729
Prenatal Exposure to a Climate-Related Disaster Results in Changes of the Placental Transcriptome and Infant Temperament.
Frontiers in genetics
2022; 13: 887619
Maternal stress during pregnancy exerts long-term effects on the mental well-being of the offspring. However, the long-term effect of prenatal exposure on the offspring's mental status is only partially understood. The placenta plays a vital role in connecting the maternal side to the fetus, thereby serving as an important interface between maternal exposure and fetal development. Here, we profiled the placental transcriptome of women who were pregnant during a hurricane (Superstorm Sandy), which struck New York City in 2012. The offspring were followed longitudinally and their temperament was assessed during the first 6-12months of age. The data identified a significant correlation between a Superstorm Sandy stress factor score and infant temperament. Further, analysis of the placental transcriptomes identified an enrichment of functional pathways related to inflammation, extracellular matrix integrity and sensory perception in the specimen from those infants with "Slow-to-Warm-up" temperament during the first year of life. Together, these findings provide initial evidence that maternal exposure to climate-related disasters results in altered placental transcriptome, which may be related to long-term emotional and behavioral consequences in children.
View details for DOI 10.3389/fgene.2022.887619
View details for PubMedID 35571026
Maternal stress and its consequences - biological strain.
American journal of perinatology
Understanding the role of stress in pregnancy and its consequences is important, particularly given documented associations between maternal stress and preterm birth and other pathologic outcomes. Physical and psychological stressors can elicit the same biological responses, known as biological strain. Chronic stressors, like poverty and racism (race-based discriminatory treatment), may create a legacy or trajectory of biological strain that no amount of coping can relieve in the absence of larger-scale socio-behavioral or societal changes. An integrative approach that takes into consideration simultaneously social and biological determinants of stress may provide the best insights into risk for preterm birth. The most successful computational approaches and the most predictive machine-learning models are likely to be those that combine information about the stressors and the biological strain (for example, as measured by different omics) experienced during pregnancy.
View details for DOI 10.1055/a-1798-1602
View details for PubMedID 35292943
Placental Gene Expression and Offspring Temperament Trajectories: Predicting Negative Affect in Early Childhood
JOURNAL OF ABNORMAL CHILD PSYCHOLOGY
2020; 48 (6): 783-795
Exposure to prenatal stress increases offspring risk for long-term neurobehavioral impairments and psychopathology, such as Attention Deficit Hyperactivity Disorder (ADHD). Epigenetic regulation of glucocorticoid pathway genes may be a potential underlying mechanism by which maternal conditions 'program' the fetal brain for downstream vulnerabilities. The present study aims to investigate whether mRNA expression of glucocorticoid pathway genes in the placenta predict offspring negative affect during early childhood (between 6 and 24 months). Participants include 318 mother-child dyads participating in a longitudinal birth cohort study. Placental mRNA expression of glucocorticoid pathway genes (HSD11B1, HSD11B2, NR3C1, NCOR2) were profiled and negative affect traits of the offspring were measured at 6, 12, 18, and 24 months. HSD11B1 mRNA expression significantly predicted negative affect (β = -.09, SE = .04; p = .036), and Distress to Limitations trajectories (β = -.13, SE = .06; p = .016). NCOR2 mRNA expression significantly predicted Distress to Limitations (β = .43, SE = .21; p = .047), and marginally predicted Sadness trajectories (β = .39, SE = .21; p = .068). HSD11B2 and NR3C1 did not predict trajectories of Negative Affect or subscale scores. Infant negative affect traits were assessed via maternal self-report, and deviated from linearity across follow-up. mRNA expression of glucocorticoid pathway genes in the placenta may be a potentially novel tool for early identification of infants at greater risk for elevated negative affect. Further study is needed to validate the utility of mRNA expression of glucocorticoid pathway genes in the placenta.
View details for DOI 10.1007/s10802-020-00632-9
View details for Web of Science ID 000520660800001
View details for PubMedID 32185610
View details for PubMedCentralID PMC7242121
The children of Superstorm Sandy: Maternal prenatal depression blunts offspring electrodermal activity
2019; 146: 107716
We set out to examine the relations between prenatal exposure to the natural disaster Superstorm Sandy, maternal depression, and offspring electrodermal activity (EDA). EDA was measured via skin conductance response (SCR) magnitude in 198 children (M = 42.54 months, SD = 12.76) during a startle paradigm. In keeping with prior research, we expected prenatal depression to be associated with hyporeactive EDA and prenatal stress to be associated with hyperreactive EDA. SCR magnitude was lower in children prenatally exposed to depression alone, when compared to Superstorm Sandy, and controls. SCR magnitude of children prenatally exposed to both maternal depression and the storm was lower than that of all other groups. Our results emphasize the influence of maternal prenatal mental health, support targeted risk assessment for children who experienced an adverse prenatal environment, and highlight the need for a deeper understanding of the interactions between maternal mood and stress on the developing child.
View details for DOI 10.1016/j.biopsycho.2019.107716
View details for Web of Science ID 000485784700010
View details for PubMedID 31176750
View details for PubMedCentralID PMC6718305
Influence of in utero exposure to maternal depression and natural disaster-related stress on infant temperament at 6 months: The children of Superstorm Sandy
INFANT MENTAL HEALTH JOURNAL
2019; 40 (2): 204-216
This study examined the effects of in utero exposure to maternal depression and Superstorm Sandy, a hurricane that hit metropolitan New York in 2012, on infant temperament at 6 months. Temperament was assessed using the Infant Behavior Questionnaire-Revised. Maternal depression was measured by the Edinburgh Postnatal Depression Scale. The main effects and the interaction of maternal depression and Sandy exposure on infant temperament were examined using a multivariable generalized linear model. Results show that prenatal maternal depression was associated with lower emotion regulation and greater distress. Stratification and interaction analyses suggested that the adverse effects of prenatal maternal depression on problematic temperament were amplified by in utero Sandy exposure. This study underscores the importance of providing prenatal screening and treatment for maternal depression during pregnancy while also identifying high-risk families who may have suffered from disaster-related traumas to provide necessary services. As the frequency of natural disasters may increase due to climate change, it is important to understand the consequences of in utero stress on child development and to formulate plans for early identification.
View details for DOI 10.1002/imhj.21766
View details for Web of Science ID 000461054900003
View details for PubMedID 30723931
View details for PubMedCentralID PMC6491203
Infant Temperament: Repercussions of Superstorm Sandy-Related Maternal Stress
CHILD PSYCHIATRY & HUMAN DEVELOPMENT
2019; 50 (1): 150-162
This study recruited a prospective cohort of 380 pregnant women before, during, or after Superstorm Sandy in 2012 to examine the association between disaster-related pre- and post-natal maternal stress and offspring temperament at 6 months-old. Mothers prospectively reported stressful experiences during the storm and rated their child's temperament 6 months postpartum. Results indicated that length of time without phone or electricity and financial loss was associated with offspring negative affect, whereas financial loss and threat of death or injury was associated with emotion dysregulation. Furthermore, offspring born before the storm had greater negative affect and lower emotion regulation than those born after the storm. Given the probable increase in the occurrence of natural disasters due to climate change in recent years (McCarthy, Intergovernmental Panel on Climate Change, Climate change 2001: impacts, adaptation, and vulnerability: contribution of Working Group II to the third assessment report of the Intergovernmental Panel on Climate Change, Cambridge University Press, Cambridge, 2001), our results highlight the necessity of education and planning to help ameliorate any potential consequences on the developing infant.
View details for DOI 10.1007/s10578-018-0828-2
View details for Web of Science ID 000458372000014
View details for PubMedID 30030653
View details for PubMedCentralID PMC6339835
Sex differences in the relations between infant temperament and electrodermal responses in early childhood
INTERNATIONAL JOURNAL OF BEHAVIORAL DEVELOPMENT
2018; 42 (6): 535-542
The present study examines the relationship between sex, infant temperament, and childhood psychophysiological reactivity via electrodermal activity (EDA). Both temperament and EDA are known to be relatively stable traits across the lifespan reflecting individual reactivity and regulation linked to suboptimal behavioral development and risk for psychopathology. However, little is known about the role of sex in the relationship between temperament and EDA. As a part of a larger longitudinal study of behavioral development, 125 participants were followed from birth till 3 years-old to examine the relationship between temperament and psychophysiological reactivity in different gender groups. Measurements of temperament at 6 months-old, and EDA, via skin conductance response (SCR) rate to a series of six startling auditory stimuli at 3 years-old were collected. Median splits of SCR scores and three temperament dimensions (positive affect, negative affect, and regulation) were created to designate high/low groups. Results indicate sex moderated the relationships between temperament traits and SCR rates. Specifically, low positive affect was associated with an increased risk for high psychophysiological reactivity in boys (odds ratio = 3.8), whereas high regulation was associated with an increased risk for greater reactivity in girls (odds ratio = 4.2). While preliminary, these findings suggest the importance of sex in relation to psychophysiological and temperamental reactivity, risk factors for developmental psychopathology. As our participants age, follow-up research to investigate the stability of these associations will provide valuable insights for the potential of EDA as a psychophysiological marker for developmental psychopathology risk in young children.
View details for DOI 10.1177/0165025418757705
View details for Web of Science ID 000452308400002
View details for PubMedID 31105363
View details for PubMedCentralID PMC6516783
Prenatal exposure to disaster-related traumatic stress and developmental trajectories of temperament in early childhood: Superstorm Sandy pregnancy study
JOURNAL OF AFFECTIVE DISORDERS
2018; 234: 335-345
Little is known about the impact of prenatal maternal stress (PNMS) on the developmental trajectory of temperament and few studies have been able to incorporate a natural disaster as a quasi-experimental stressor. The current study investigated PNMS related to Superstorm Sandy ('Sandy'), a hurricane that struck the New York metropolitan area in October 2012, in terms of objective exposure during pregnancy, subjective stress reaction as assessed by maternal symptoms of post-traumatic stress, and their impact on the developmental changes in temperament during early childhood.A subsample of 318 mother-child dyads was drawn from the Stress in Pregnancy Study. Temperament was measured at 6, 12, 18, and 24 months of age.Objective exposure was associated with greater High-Intensity Pleasure, Approach, Perceptual Sensitivity and Fearfulness, but lower Cuddliness and Duration of Orientation at 6 months. Objective exposure and its interaction with subjective stress reaction predicted developmental changes in temperament. In particular, objective exposure was linked to greater increases in Activity Level but decreases in High-Intensity Pleasure, Approach, and Fearfulness. The combination of objective exposure and subjective stress reaction was also associated with greater increases in Activity Level.Temperament was measured solely via maternal report. Trimester-specific effects of Sandy on temperament were not examined.This is the first study to examine the effects of prenatal maternal exposure to a natural disaster on trajectories of early childhood temperament. Findings suggest that both objective stress exposure and subjective stress reaction in-utero predict developmental trajectories of temperament in early childhood.
View details for DOI 10.1016/j.jad.2018.02.067
View details for Web of Science ID 000429308000049
View details for PubMedID 29614461
View details for PubMedCentralID PMC5963732
Placental MAOA expression mediates prenatal stress effects on temperament in 12-month-olds
INFANT AND CHILD DEVELOPMENT
2018; 27 (4)
The placenta adapts to maternal environment and its alterations may have a lasting impact on child's temperament development. Prenatal stress has been linked to both a downregulation of monoamine oxidase A (MAOA) gene expression in the placenta and to difficult temperament. Capitalizing on an ongoing longitudinal study, we analysed data from 95 mother-child dyads to investigate whether MAOA mediates the association between prenatal stress and infant temperament. Prenatal stress was defined as exposure to Superstorm Sandy (Sandy) during pregnancy. Infant temperament was measured by Infant Behaviour Questionnaire-Revised. MAOA gene expression was quantified in placenta tissue. The Smiling and Laughter subscale score was independently associated with Sandy exposure and MAOA placental gene expression. Mediation analysis confirmed that MAOA expression partially mediated the relationship between Sandy and Smiling and Laughter subscale, suggesting that in utero exposure to Sandy could induce lower frequency of smiling and laughter via downregulation of placental MAOA gene expression. These effects could compromise optimal temperamental trajectory and contribute to risk for psychological problems. Placental epigenetic markers can contribute to a multidimensional model of early intervention for high-risk children.
View details for DOI 10.1002/icd.2094
View details for Web of Science ID 000440923300011
View details for PubMedID 30505241
View details for PubMedCentralID PMC6261505
Timing of prenatal exposure to trauma and altered placental expressions of hypothalamic-pituitary-adrenal axis genes and genes driving neurodevelopment
JOURNAL OF NEUROENDOCRINOLOGY
2018; 30 (4): e12581
Prenatal maternal stress increases the risk for negative developmental outcomes in offspring; however, the underlying biological mechanisms remain largely unexplored. In the present study, alterations in placental gene expression associated with maternal stress were examined to clarify the potential underlying epi/genetic mechanisms. Expression levels of 40 selected genes involved in regulating foetal hypothalamic-pituitary-adrenal axis and neurodevelopment were profiled in placental tissues collected from a birth cohort established around the time of Superstorm Sandy. Objective prenatal traumatic stress was defined as whether mothers were exposed to Superstorm Sandy during pregnancy. Among the 275 mother-infant dyads, 181 dyads were delivered before Superstorm Sandy (ie, Control), 66 dyads were exposed to Superstorm Sandy during the first trimester (ie, Early Exposure) and 28 were exposed to Superstorm Sandy during the second or third trimester (ie, Mid-Late Exposure). Across all trimesters, expression of HSD11B2, MAOA, ZNF507 and DYRK1A was down-regulated among those exposed to Superstorm Sandy during pregnancy. Furthermore, trimester-specific differences were also observed: exposure during early gestation was associated with down-regulation of HSD11B1 and MAOB and up-regulation of CRHBP; exposure during mid-late gestation was associated with up-regulation of SRD5A3. The findings of the present study suggest that placental gene expression may be altered in response to traumatic stress exposure during pregnancy, and the susceptibility of these genes is dependent on the time of the exposure during pregnancy. Further studies should aim to clarify the biological mechanisms that underlie trimester-specific exposure by evaluating the differential impact on offspring neurodevelopment later in childhood.
View details for DOI 10.1111/jne.12581
View details for Web of Science ID 000430917800003
View details for PubMedID 29423924
View details for PubMedCentralID PMC5939590
Neurodevelopmental consequences in offspring of mothers with preeclampsia during pregnancy: underlying biological mechanism via imprinting genes
ARCHIVES OF GYNECOLOGY AND OBSTETRICS
2017; 295 (6): 1319-1329
Preeclampsia is known to be a leading cause of mortality and morbidity among mothers and their infants. Approximately 3-8% of all pregnancies in the US are complicated by preeclampsia and another 5-7% by hypertensive symptoms. However, less is known about its long-term influence on infant neurobehavioral development. The current review attempts to demonstrate new evidence for imprinting gene dysregulation caused by hypertension, which may explain the link between maternal preeclampsia and neurocognitive dysregulation in offspring.Pub Med and Web of Science databases were searched using the terms "preeclampsia," "gestational hypertension," "imprinting genes," "imprinting dysregulation," and "epigenetic modification," in order to review the evidence demonstrating associations between preeclampsia and suboptimal child neurodevelopment, and suggest dysregulation of placental genomic imprinting as a potential underlying mechanism.The high mortality and morbidity among mothers and fetuses due to preeclampsia is well known, but there is little research on the long-term biological consequences of preeclampsia and resulting hypoxia on the fetal/child neurodevelopment. In the past decade, accumulating evidence from studies that transcend disciplinary boundaries have begun to show that imprinted genes expressed in the placenta might hold clues for a link between preeclampsia and impaired cognitive neurodevelopment. A sudden onset of maternal hypertension detected by the placenta may result in misguided biological programming of the fetus via changes in the epigenome, resulting in suboptimal infant development.Furthering our understanding of the molecular and cellular mechanisms through which neurodevelopmental trajectories of the fetus/infant are affected by preeclampsia and hypertension will represent an important first step toward preventing adverse neurodevelopment in infants.
View details for DOI 10.1007/s00404-017-4347-3
View details for Web of Science ID 000401337700004
View details for PubMedID 28382413
View details for PubMedCentralID PMC6058691