Annual Research Review: Neuroimmune network model of depression: a developmental perspective / Robin NUSSLOCK in Journal of Child Psychology and Psychiatry, 65-4 (April 2024)  

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 65-4 (April 2024) . - p.538-567 Titre : Annual Research Review: Neuroimmune network model of depression: a developmental perspective Type de document : Texte imprimé et/ou numérique Auteurs : Robin NUSSLOCK, Auteur ; Lauren B. ALLOY, Auteur ; Gene H. BRODY, Auteur ; Gregory E. MILLER, Auteur Article en page(s) : p.538-567 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Depression is a serious public health problem, and adolescence is an 'age of risk' for the onset of Major Depressive Disorder. Recently, we and others have proposed neuroimmune network models that highlight bidirectional communication between the brain and the immune system in both mental and physical health, including depression. These models draw on research indicating that the cellular actors (particularly monocytes) and signaling molecules (particularly cytokines) that orchestrate inflammation in the periphery can directly modulate the structure and function of the brain. In the brain, inflammatory activity heightens sensitivity to threats in the cortico-amygdala circuit, lowers sensitivity to rewards in the cortico-striatal circuit, and alters executive control and emotion regulation in the prefrontal cortex. When dysregulated, and particularly under conditions of chronic stress, inflammation can generate feelings of dysphoria, distress, and anhedonia. This is proposed to initiate unhealthy, self-medicating behaviors (e.g. substance use, poor diet) to manage the dysphoria, which further heighten inflammation. Over time, dysregulation in these brain circuits and the inflammatory response may compound each other to form a positive feedback loop, whereby dysregulation in one organ system exacerbates the other. We and others suggest that this neuroimmune dysregulation is a dynamic joint vulnerability for depression, particularly during adolescence. We have three goals for the present paper. First, we extend neuroimmune network models of mental and physical health to generate a developmental framework of risk for the onset of depression during adolescence. Second, we examine how a neuroimmune network perspective can help explain the high rates of comorbidity between depression and other psychiatric disorders across development, and multimorbidity between depression and stress-related medical illnesses. Finally, we consider how identifying neuroimmune pathways to depression can facilitate a 'next generation' of behavioral and biological interventions that target neuroimmune signaling to treat, and ideally prevent, depression in youth and adolescents. En ligne : https://doi.org/10.1111/jcpp.13961 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=523 [article] Annual Research Review: Neuroimmune network model of depression: a developmental perspective [Texte imprimé et/ou numérique] / Robin NUSSLOCK, Auteur ; Lauren B. ALLOY, Auteur ; Gene H. BRODY, Auteur ; Gregory E. MILLER, Auteur . - p.538-567. Langues : Anglais (eng) in Journal of Child Psychology and Psychiatry > 65-4 (April 2024) . - p.538-567 Index. décimale : PER Périodiques Résumé : Depression is a serious public health problem, and adolescence is an 'age of risk' for the onset of Major Depressive Disorder. Recently, we and others have proposed neuroimmune network models that highlight bidirectional communication between the brain and the immune system in both mental and physical health, including depression. These models draw on research indicating that the cellular actors (particularly monocytes) and signaling molecules (particularly cytokines) that orchestrate inflammation in the periphery can directly modulate the structure and function of the brain. In the brain, inflammatory activity heightens sensitivity to threats in the cortico-amygdala circuit, lowers sensitivity to rewards in the cortico-striatal circuit, and alters executive control and emotion regulation in the prefrontal cortex. When dysregulated, and particularly under conditions of chronic stress, inflammation can generate feelings of dysphoria, distress, and anhedonia. This is proposed to initiate unhealthy, self-medicating behaviors (e.g. substance use, poor diet) to manage the dysphoria, which further heighten inflammation. Over time, dysregulation in these brain circuits and the inflammatory response may compound each other to form a positive feedback loop, whereby dysregulation in one organ system exacerbates the other. We and others suggest that this neuroimmune dysregulation is a dynamic joint vulnerability for depression, particularly during adolescence. We have three goals for the present paper. First, we extend neuroimmune network models of mental and physical health to generate a developmental framework of risk for the onset of depression during adolescence. Second, we examine how a neuroimmune network perspective can help explain the high rates of comorbidity between depression and other psychiatric disorders across development, and multimorbidity between depression and stress-related medical illnesses. Finally, we consider how identifying neuroimmune pathways to depression can facilitate a 'next generation' of behavioral and biological interventions that target neuroimmune signaling to treat, and ideally prevent, depression in youth and adolescents. En ligne : https://doi.org/10.1111/jcpp.13961 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=523

Childhood abuse and neglect and physical health at midlife: Prospective, longitudinal evidence / William F. JOHNSON in Development and Psychopathology, 29-5 (December 2017)  

Public ISBD [article]  inDevelopment and Psychopathology > 29-5 (December 2017) . - p.1935-1946 Titre : Childhood abuse and neglect and physical health at midlife: Prospective, longitudinal evidence Type de document : Texte imprimé et/ou numérique Auteurs : William F. JOHNSON, Auteur ; Chloe O. HUELSNITZ, Auteur ; Elizabeth A. CARLSON, Auteur ; Glenn I. ROISMAN, Auteur ; Michelle M. ENGLUND, Auteur ; Gregory E. MILLER, Auteur ; Jeffry A. SIMPSON, Auteur Article en page(s) : p.1935-1946 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Previous research suggests that the experience of abuse and neglect in childhood has negative implications for physical health in adulthood. Using data from the Minnesota Longitudinal Study of Risk and Adaptation (N = 115), the present research examined the predictive significance of childhood physical abuse, sexual abuse, and physical/cognitive neglect for multilevel assessments of physical health at midlife (age 37–39 years), including biomarkers of cardiometabolic risk, self-reports of quality of health, and a number of health problems. Analyses revealed that childhood physical/cognitive neglect, but not physical or sexual abuse, predicted all three health outcomes in middle adulthood, even when controlling for demographic risk factors and adult health maintenance behaviors. We discuss possible explanations for the unique significance of neglect in this study and suggest future research that could clarify previous findings regarding the differential impact of different types of abuse and neglect on adult health. En ligne : http://dx.doi.org/10.1017/S095457941700150X Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=324 [article] Childhood abuse and neglect and physical health at midlife: Prospective, longitudinal evidence [Texte imprimé et/ou numérique] / William F. JOHNSON, Auteur ; Chloe O. HUELSNITZ, Auteur ; Elizabeth A. CARLSON, Auteur ; Glenn I. ROISMAN, Auteur ; Michelle M. ENGLUND, Auteur ; Gregory E. MILLER, Auteur ; Jeffry A. SIMPSON, Auteur . - p.1935-1946. Langues : Anglais (eng) in Development and Psychopathology > 29-5 (December 2017) . - p.1935-1946 Index. décimale : PER Périodiques Résumé : Previous research suggests that the experience of abuse and neglect in childhood has negative implications for physical health in adulthood. Using data from the Minnesota Longitudinal Study of Risk and Adaptation (N = 115), the present research examined the predictive significance of childhood physical abuse, sexual abuse, and physical/cognitive neglect for multilevel assessments of physical health at midlife (age 37–39 years), including biomarkers of cardiometabolic risk, self-reports of quality of health, and a number of health problems. Analyses revealed that childhood physical/cognitive neglect, but not physical or sexual abuse, predicted all three health outcomes in middle adulthood, even when controlling for demographic risk factors and adult health maintenance behaviors. We discuss possible explanations for the unique significance of neglect in this study and suggest future research that could clarify previous findings regarding the differential impact of different types of abuse and neglect on adult health. En ligne : http://dx.doi.org/10.1017/S095457941700150X Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=324

Family-centered prevention ameliorates the longitudinal association between risky family processes and epigenetic aging / Gene H. BRODY in Journal of Child Psychology and Psychiatry, 57-5 (May 2016)  

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 57-5 (May 2016) . - p.566-574 Titre : Family-centered prevention ameliorates the longitudinal association between risky family processes and epigenetic aging Type de document : Texte imprimé et/ou numérique Auteurs : Gene H. BRODY, Auteur ; Tianyi YU, Auteur ; Edith CHEN, Auteur ; Steven R. H. BEACH, Auteur ; Gregory E. MILLER, Auteur Article en page(s) : p.566-574 Langues : Anglais (eng) Mots-clés : Depression  epigenetics  epigenetic clock  health  intervention  parenting  prevention Index. décimale : PER Périodiques Résumé : Background Research has suggested that ‘risky’ family processes have unforeseen negative consequences for health later in life. The purpose of this study was to further understanding of risky family environments and development of health vulnerabilities by (a) examining the likelihood that elevated levels of parental depressive symptoms when children are age 11 forecast accelerated epigenetic aging 9 years later at age 20; (b) determining whether participation in an efficacious family-centered prevention program focused on enhancing supportive parenting and strengthening family relationships will ameliorate this association; and (c) testing a moderation-mediation hypothesis that prevention-induced reductions in harsh parenting across adolescence will account for prevention effects in reducing accelerated epigenetic aging. Methods In the rural southeastern United States, parents and 11-year-old children from 399 families participated in the Strong African American Families (SAAF) program or a control condition. Parents reported their own depressive symptoms when their children were 11, and both youths and parents reported youth exposure to harsh parenting at ages 11 and 16. Blood was drawn from youths at age 20 to measure accelerated epigenetic aging using a marker derived from the DNA methylation of cells. Results Elevated parental depressive symptoms forecast accelerated epigenetic aging among youths in the control condition, but not among SAAF participants. Moderated-mediation analyses confirmed that reductions in harsh parenting accounted for SAAF's protective effects on epigenetic aging. Subsequent exploratory analyses indicated that accelerated epigenetic aging forecast emotional distress among young adults in the control condition but not among those who participated in SAAF. Conclusions This study is unique in using a randomized prevention trial to test hypotheses about the ways risky family processes contribute to accelerated epigenetic aging. The results suggest that developmentally appropriate family-centered interventions designed to enhance parenting and strengthen families can buffer the biological residue of life in a risky family. En ligne : http://dx.doi.org/10.1111/jcpp.12495 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=288 [article] Family-centered prevention ameliorates the longitudinal association between risky family processes and epigenetic aging [Texte imprimé et/ou numérique] / Gene H. BRODY, Auteur ; Tianyi YU, Auteur ; Edith CHEN, Auteur ; Steven R. H. BEACH, Auteur ; Gregory E. MILLER, Auteur . - p.566-574. Langues : Anglais (eng) in Journal of Child Psychology and Psychiatry > 57-5 (May 2016) . - p.566-574 Mots-clés : Depression  epigenetics  epigenetic clock  health  intervention  parenting  prevention Index. décimale : PER Périodiques Résumé : Background Research has suggested that ‘risky’ family processes have unforeseen negative consequences for health later in life. The purpose of this study was to further understanding of risky family environments and development of health vulnerabilities by (a) examining the likelihood that elevated levels of parental depressive symptoms when children are age 11 forecast accelerated epigenetic aging 9 years later at age 20; (b) determining whether participation in an efficacious family-centered prevention program focused on enhancing supportive parenting and strengthening family relationships will ameliorate this association; and (c) testing a moderation-mediation hypothesis that prevention-induced reductions in harsh parenting across adolescence will account for prevention effects in reducing accelerated epigenetic aging. Methods In the rural southeastern United States, parents and 11-year-old children from 399 families participated in the Strong African American Families (SAAF) program or a control condition. Parents reported their own depressive symptoms when their children were 11, and both youths and parents reported youth exposure to harsh parenting at ages 11 and 16. Blood was drawn from youths at age 20 to measure accelerated epigenetic aging using a marker derived from the DNA methylation of cells. Results Elevated parental depressive symptoms forecast accelerated epigenetic aging among youths in the control condition, but not among SAAF participants. Moderated-mediation analyses confirmed that reductions in harsh parenting accounted for SAAF's protective effects on epigenetic aging. Subsequent exploratory analyses indicated that accelerated epigenetic aging forecast emotional distress among young adults in the control condition but not among those who participated in SAAF. Conclusions This study is unique in using a randomized prevention trial to test hypotheses about the ways risky family processes contribute to accelerated epigenetic aging. The results suggest that developmentally appropriate family-centered interventions designed to enhance parenting and strengthen families can buffer the biological residue of life in a risky family. En ligne : http://dx.doi.org/10.1111/jcpp.12495 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=288

Harsh parent–child conflict is associated with decreased anti-inflammatory gene expression and increased symptom severity in children with asthma / Katherine B. EHRLICH in Development and Psychopathology, 27-4 (Part 2) (November 2015)  

Public ISBD [article]  inDevelopment and Psychopathology > 27-4 (Part 2) (November 2015) . - p.1547-1554 Titre : Harsh parent–child conflict is associated with decreased anti-inflammatory gene expression and increased symptom severity in children with asthma Type de document : Texte imprimé et/ou numérique Auteurs : Katherine B. EHRLICH, Auteur ; Gregory E. MILLER, Auteur ; Edith CHEN, Auteur Article en page(s) : p.1547-1554 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Asthma is a chronic respiratory disorder that affects over 7 million children in the United States. Evidence indicates that family stressors are associated with worsening of asthma symptoms, and some research suggests that these stressful experiences engender changes in children's immune systems in ways that exacerbate airway inflammation and contribute to both acute and chronic asthma symptoms. We examined the association between observed experiences of parent–child conflict and the expression of signaling molecules involved in the transduction of anti-inflammatory signals that regulate airway inflammation and obstruction. Fifty-seven children and their parents participated in a conflict task, and coders rated interactions for evidence of harsh and supportive behaviors. Children reported on their perceptions of parental support and reported on their daily asthma symptoms for 2 weeks. We collected peripheral blood in children to measure leukocyte expression of messenger RNA for the glucocorticoid receptor and the ?2-adrenergic receptor. Analyses revealed that harsh conflict behaviors were associated with decreased expression of both messenger RNAs and more severe asthma symptoms. Neither supportive behaviors nor perceived parental support was associated with gene expression or asthma symptoms. These findings suggest that harsh interactions with parents are associated with downregulation of key anti-inflammatory signaling molecules and difficulties breathing in children with asthma. Children with asthma who are also victims of maltreatment may be particularly susceptible to transcriptional changes in immune cells that could worsen asthma over time. En ligne : http://dx.doi.org/10.1017/S0954579415000930 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=273 [article] Harsh parent–child conflict is associated with decreased anti-inflammatory gene expression and increased symptom severity in children with asthma [Texte imprimé et/ou numérique] / Katherine B. EHRLICH, Auteur ; Gregory E. MILLER, Auteur ; Edith CHEN, Auteur . - p.1547-1554. Langues : Anglais (eng) in Development and Psychopathology > 27-4 (Part 2) (November 2015) . - p.1547-1554 Index. décimale : PER Périodiques Résumé : Asthma is a chronic respiratory disorder that affects over 7 million children in the United States. Evidence indicates that family stressors are associated with worsening of asthma symptoms, and some research suggests that these stressful experiences engender changes in children's immune systems in ways that exacerbate airway inflammation and contribute to both acute and chronic asthma symptoms. We examined the association between observed experiences of parent–child conflict and the expression of signaling molecules involved in the transduction of anti-inflammatory signals that regulate airway inflammation and obstruction. Fifty-seven children and their parents participated in a conflict task, and coders rated interactions for evidence of harsh and supportive behaviors. Children reported on their perceptions of parental support and reported on their daily asthma symptoms for 2 weeks. We collected peripheral blood in children to measure leukocyte expression of messenger RNA for the glucocorticoid receptor and the ?2-adrenergic receptor. Analyses revealed that harsh conflict behaviors were associated with decreased expression of both messenger RNAs and more severe asthma symptoms. Neither supportive behaviors nor perceived parental support was associated with gene expression or asthma symptoms. These findings suggest that harsh interactions with parents are associated with downregulation of key anti-inflammatory signaling molecules and difficulties breathing in children with asthma. Children with asthma who are also victims of maltreatment may be particularly susceptible to transcriptional changes in immune cells that could worsen asthma over time. En ligne : http://dx.doi.org/10.1017/S0954579415000930 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=273

Harshness and unpredictability: Childhood environmental links with immune and asthma outcomes / Phoebe H. LAM in Development and Psychopathology, 34-2 (May 2022)  

Public ISBD [article]  inDevelopment and Psychopathology > 34-2 (May 2022) . - 587-596 Titre : Harshness and unpredictability: Childhood environmental links with immune and asthma outcomes Type de document : Texte imprimé et/ou numérique Auteurs : Phoebe H. LAM, Auteur ; Gregory E. MILLER, Auteur ; Lauren HOFFER, Auteur ; Rebekah SILIEZAR, Auteur ; Johanna DEZIL, Auteur ; Amanda MCDONALD, Auteur ; Edith CHEN, Auteur Article en page(s) : 587-596 Langues : Anglais (eng) Mots-clés : asthma  harshness  inflammation  unpredictability Index. décimale : PER Périodiques Résumé : The environment has pervasive impacts on human development, and two key environmental conditions ? harshness and unpredictability ? are proposed to be instrumental in tuning development. This study examined (1) how harsh and unpredictable environments related to immune and clinical outcomes in the context of childhood asthma, and (2) whether there were independent associations of harshness and unpredictability with these outcomes. Participants were 290 youth physician-diagnosed with asthma. Harshness was assessed with youth-reported exposure to violence and neighborhood-level murder rate. Unpredictability was assessed with parent reports of family structural changes. Youth also completed measures of asthma control as well as asthma quality of life and provided blood samples to assess immune profiles, including in vitro cytokine responses to challenge and sensitivity to inhibitory signals from glucocorticoids. Results indicated that harshness was associated with more pronounced pro-inflammatory cytokine production following challenge and less sensitivity to the inhibitory properties of glucocorticoids. Furthermore, youth exposed to harsher environments reported less asthma control and poorer quality of life. All associations with harshness persisted when controlling for unpredictability. No associations between unpredictability and outcomes were found. These findings suggest that relative to unpredictability, harshness may be a more consistent correlate of asthma-relevant immune and clinical outcomes. En ligne : http://dx.doi.org/10.1017/s0954579421001577 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=474 [article] Harshness and unpredictability: Childhood environmental links with immune and asthma outcomes [Texte imprimé et/ou numérique] / Phoebe H. LAM, Auteur ; Gregory E. MILLER, Auteur ; Lauren HOFFER, Auteur ; Rebekah SILIEZAR, Auteur ; Johanna DEZIL, Auteur ; Amanda MCDONALD, Auteur ; Edith CHEN, Auteur . - 587-596. Langues : Anglais (eng) in Development and Psychopathology > 34-2 (May 2022) . - 587-596 Mots-clés : asthma  harshness  inflammation  unpredictability Index. décimale : PER Périodiques Résumé : The environment has pervasive impacts on human development, and two key environmental conditions ? harshness and unpredictability ? are proposed to be instrumental in tuning development. This study examined (1) how harsh and unpredictable environments related to immune and clinical outcomes in the context of childhood asthma, and (2) whether there were independent associations of harshness and unpredictability with these outcomes. Participants were 290 youth physician-diagnosed with asthma. Harshness was assessed with youth-reported exposure to violence and neighborhood-level murder rate. Unpredictability was assessed with parent reports of family structural changes. Youth also completed measures of asthma control as well as asthma quality of life and provided blood samples to assess immune profiles, including in vitro cytokine responses to challenge and sensitivity to inhibitory signals from glucocorticoids. Results indicated that harshness was associated with more pronounced pro-inflammatory cytokine production following challenge and less sensitivity to the inhibitory properties of glucocorticoids. Furthermore, youth exposed to harsher environments reported less asthma control and poorer quality of life. All associations with harshness persisted when controlling for unpredictability. No associations between unpredictability and outcomes were found. These findings suggest that relative to unpredictability, harshness may be a more consistent correlate of asthma-relevant immune and clinical outcomes. En ligne : http://dx.doi.org/10.1017/s0954579421001577 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=474

One size does not fit all: Links between shift-and-persist and asthma in youth are moderated by perceived social status and experience of unfair treatment / Phoebe H. LAM in Development and Psychopathology, 30-5 (December 2018)  

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Resilience in children with chronic illness: Tests of the shift-and-persist and skin-deep resilience theories / Michelle A. CHEN ; Rachel Y. CHIU ; Tao JIANG ; Gregory E. MILLER in Development and Psychopathology, 35-5 (December 2023)  

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Smoking in young adulthood among African Americans: Interconnected effects of supportive parenting in early adolescence, proinflammatory epitype, and young adult stress / Steven R. H. BEACH in Development and Psychopathology, 29-3 (August 2017)  

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Social encounters in daily life and 2-year changes in metabolic risk factors in young women / Kharah ROSS in Development and Psychopathology, 23-3 (August 2011)  

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Socioeconomic disadvantage and high-effort coping in childhood: evidence of skin-deep resilience / Sarah M. LYLE ; Kelsey L. CORALLO ; Julie M. BRISSON ; Elizabeth R. WIGGINS ; Tianyi YU ; Edith CHEN ; Gregory E. MILLER ; Gene H. BRODY in Journal of Child Psychology and Psychiatry, 65-3 (March 2023)  

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Testing the biological embedding hypothesis: Is early life adversity associated with a later proinflammatory phenotype? / Katherine B. EHRLICH in Development and Psychopathology, 28-4 pt2 (November 2016)  

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Threat vigilance and socioeconomic disparities in metabolic health / Camelia E. HOSTINAR in Development and Psychopathology, 29-5 (December 2017)  

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Trajectories of relationship stress and inflammatory processes in adolescence / Katherine B. EHRLICH in Development and Psychopathology, 28-1 (February 2016)  

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Youth temperament, harsh parenting, and variation in the oxytocin receptor gene forecast allostatic load during emerging adulthood / Gene H. BRODY in Development and Psychopathology, 29-3 (August 2017)  

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