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NOBEL PRIZE 2026

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NIHEUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENTF31

Maternal-Child RSA Synchrony in Infants with Fragile X Syndrome

Active
Institution
University of South Carolina at Columbia, SC
Principal investigator
Rachel Hantman
Funding
$43K
Duration
2024–2027
Open portfolio

Moonbase score

Still being scored

Abstract

PROJECT SUMMARY/ABSTRACT Maternal-child synchrony describes the temporal associations between maternal and child social and physiological states, often occurring within maternal-child interactions. Maternal-child synchrony is a critical component of child development that emerges during pregnancy and is present throughout childhood. The quality of maternal-child synchrony is associated with future social development, making it an important construct to understand. Given its developmental importance, it is critical to characterize maternal-child synchrony in specific subgroups vulnerable to weakened maternal-child synchrony. It is well established that maternal-child physiological synchrony decreases in clinical samples, such as when mothers are experiencing mental health challenges (e.g., anxiety, depression) and when children themselves belong to at-risk groups (e.g., prematurity), but this association is poorly understood in neurodevelopmental disorders, like fragile X syndrome (FXS). FXS is a rare, monogenetic disorder, characterized by deficits in attention, social development, and emotional regulation. These deficits have been attributed to physiological hyperarousal. This “hyperarousal hypothesis” of FXS has been demonstrated via cardiac activity, particularly when indexed by respiratory sinus arrythmia (RSA), wherein individuals with FXS have shown depressed RSA (thereby indicating physiological arousal) when neurotypically (NT) developing individuals have shown higher RSA. As an inherited disorder, mothers of children with FXS typically have the fragile X premutation (FXp). Women with FXp demonstrate atypical physiological arousal indexed by lower RSA as well, and they experience elevated anxiety, depression, and stress. Collectively, in FXS, these child and maternal phenotypic factors (i.e., clinical status, atypical RSA) coalesce into vulnerability to disrupted maternal-child RSA synchrony. Yet, no studies have examined maternal-child RSA synchrony in FXS or focused on infancy. Just as maternal-child synchrony is influenced by the phenotypes of the dyadic partners, mother-child interactions are influenced by contextual factors that surround the child, such as parental stress and familial relationships; this important contextual influence has also been absent from the FXS maternal-child synchrony literature. Therefore, the over-arching aim of this F31 is to examine maternal-child RSA synchrony in 12-month-old males with FXS (nFXS = 25), contrasted against male infants with neurotypical development (NT; nNT = 25) at baseline (Aim 1a) and during a standardized mother-child free play interaction task (Aim 2b). I will identify how contextual variables (i.e., parental stress, family relationships) differentially impact both baseline maternal-child RSA synchrony (Aim 1b) and maternal-child RSA synchrony during the mother-child free play task (Aim 2b) in both groups, as well as how behavioral synchrony impacts maternal-child RSA synchrony during the mother-child free play task (Aim 2c) across groups.

LOADING MOONBASE SCORE

F31EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENTSpecial Emphasis Panel[ZRG1-F16-H(20)L]contextualsynchronychildarousalfxsanxiety depressionfragile syndromefragile

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