@article{pmid41922795,

title = {Sex-specific neurodevelopmental pathways to depressive symptoms},

author = {Shi Yu Chan and Pei Huang and Zhen Ming Ngoh and Joanne S M Chia and Janice Lee and Aisleen M A Manahan and Jasmine S M Chuah and Marielle V Fortier and Fabian Yap and Yap-Seng Chong and Peter Gluckman and Johan Eriksson and Michael J Meaney and Ai Peng Tan},

doi = {10.1038/s41380-026-03576-6},

issn = {1476-5578},

year  = {2026},

date = {2026-08-01},

journal = {Mol Psychiatry},

volume = {31},

number = {8},

pages = {4563--4575},

abstract = {While sex differences in the prevalence of depression are consistently observed in adolescence, sex-specific endophenotypes associated with depression appear earlier in childhood. Our study examined whether neurodevelopmental changes in childhood associated with depressive symptoms in adolescence show sex-specificity. Longitudinal multi-modal neuroimaging data were collected at ages 4.5, 6.0, and 7.5 years. Neurodevelopment was measured by structure-function coupling (SC-FC), the correlation between structural and functional connectivity, derived for 114 cortical regions and averaged across the whole cortex. Depressive symptoms were self-reported at age 13 years with the Child Depression Inventory (CDI), Youth Self Report (YSR), and Multidimensional Anxiety Scale for Children. Partial least squares correlation was used to identify latent variables that maximized covariance between the 28 CDI items and 114 cortical regions. Females reported significantly higher depressive symptoms than males at age 13 years (N = 636, p < 0.001). Whole cortex SC-FC showed sex-specific trajectories across childhood (N = 549, 917 scans). Females showed a steeper decrease in SC-FC relative to males in the pre-school phase (ages 4.5 to 6.0, p = 0.019) but not during mid-childhood (ages 6.0 to 7.5, p = 0.340). For both childhood phases (Pre-school: N = 97, Mid-childhood: N = 162), sex-specific models better explained the data than full cohort ("All") models. Items/regions with significant contributions to their respective latent variables were distinct in males and females and between childhood phases. Sex-specific cortical changes improved regression models predicting YSR Depressive Problems. We provide evidence for sex-specific childhood neurodevelopmental pathways to depressive symptoms in adolescence that could guide the timing for more effective intervention programs.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid42532033,

title = {A cortical-hypothalamic neural circuit for compulsive eating in mice},

author = {Yi Ning Leow and Esra Senol and Xing Qian and Xiaoyu Wang and Aditya Nair and Olivia Khoo and Xiaoning Liu and Yi-Fei Li and Menghan Wang and Shivangi Sharma and Yi Zhang and Xiaodong Han and Marielle V Fortier and Michael J Meaney and Yap Seng Chong and Anna Magdalena Fogel and Keri McCrickerd and Ai Peng Tan and Fang Wang and Ti-Fei Yuan and Juan Helen Zhou and Hasan Mohammad and Yu Fu},

doi = {10.1016/j.neuron.2026.07.005},

issn = {1097-4199},

year  = {2026},

date = {2026-07-01},

journal = {Neuron},

abstract = {Binge-eating disorder (BED) is the most common eating disorder and is strongly associated with obesity. The medial prefrontal cortex (mPFC) has been implicated in compulsive behavior and is known to project to multiple hypothalamic cell types implicated in maladaptive feeding. How the mPFC engages hypothalamic networks and whether such interactions are relevant for human disease remain unknown. Here, using a binge-eating-induced compulsive eating (BiCOM) paradigm in mice, we demonstrate that rostral zona incerta γ-aminobutyric acid (GABAergic) neurons (GABA) drive compulsive eating. Manipulating either GABA neurons or their mPFC inputs bidirectionally modulated compulsive eating. In vivo imaging showed that BiCOM modified mPFC neural dynamics, creating persistent attractor states driven by, and with sustained selectivity for, palatable food. Moreover, human fMRI showed that mPFC-rostral zona incerta (rZI) connectivity correlated with body weight and binge eating. Together, these results identify a cortical-hypothalamic mechanism for compulsive eating in mice and highlight potential targets for intervention in BED and obesity.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid42491708,

title = {The Legacy of Seymour Levine},

author = {Michael J Meaney},

doi = {10.1016/j.ynstr.2026.100834},

issn = {2352-2895},

year  = {2026},

date = {2026-07-01},

journal = {Neurobiol Stress},

volume = {43},

pages = {100834},

abstract = {This essay assumes an historical perspective intended to highlight the major contributions of Seymour "Gig" Levine to the conceptual scaffold that guides so much of the current research in development and psychopathology. I suggest that perhaps Levine's most important contribution was to establish an experimental framework that served to transition the clinical observations of Freud and the attachment theories of Bowlby into modern Psychology/Psychiatry.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid41861248,

title = {Glucocorticoid Receptor-Regulated Gene Networks and Mental Health},

author = {Michael J Meaney and Elisabeth B Binder},

doi = {10.1146/annurev-neuro-102124-031826},

issn = {1545-4126},

year  = {2026},

date = {2026-07-01},

journal = {Annu Rev Neurosci},

volume = {49},

number = {1},

pages = {105--123},

abstract = {Stressors, including those occurring in early development, predict an increased risk for psychopathology. The challenge is that of defining causal pathways that connect stressful conditions to specific health outcomes and then leveraging this knowledge toward treatments. This review focuses on glucocorticoids (GCs), the end products of stressor-induced hypothalamic-pituitary-adrenal axis activity, and reviews evidence, including recent multiomics analyses, regarding their role in mental health. We outline the challenges in translating this knowledge into effective treatments and recent evidence for the potential of gene network analyses to identify molecular pathways linking stress to psychopathology. A detailed examination of GC activity through the glucocorticoid receptor is presented as an example of the complexities involved in achieving this research objective and paths to novel interventions through gene network analyses.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid41651182,

title = {Omega-3 PUFA concentrations in childhood prospectively associate with academic performance beyond a healthy diet: findings from the multiethnic Asian Growing Up in Singapore Towards healthy Outcomes cohort study},

author = {Karen Mei-Ling Tan and Jun Shi Lai and Jia Ying Toh and Yi Ying Ong and Michelle Zl Kee and Wei Wei Pang and Melvin Khee Shing Leow and Fabian Yap and Johan Gunnar Eriksson and David Cameron-Smith and Michael Meaney and Evelyn Chung Ning Law and Mary Foong-Fong Chong},

doi = {10.1016/j.ajcnut.2026.101233},

issn = {1938-3207},

year  = {2026},

date = {2026-04-01},

journal = {Am J Clin Nutr},

volume = {123},

number = {4},

pages = {101233},

abstract = {BACKGROUND: The influence of plasma DHA and overall omega-3 (n-3) long-chain PUFA (LC-PUFA) on child cognitive development is unclear.nnOBJECTIVES: We examined if plasma LC-PUFA concentrations are prospectively associated with academic performance in primary school children and if diet patterns modulate the relationship.nnMETHODS: Children were from the Growing Up in Singapore Toward healthy Outcomes cohort. Fasting LC-PUFA concentrations were measured using nuclear magnetic resonance spectroscopy at age 8 y (n = 557). Dietary patterns were derived using principal component analysis from a validated food frequency questionnaire at age 7 y. Academic performance was assessed using the Wechsler Individual Achievement Test-III at age 9 y (n = 288) and the primary school leaving examination (PSLE) at age 12 y (n = 408). The relationships of LC-PUFAs to academic performance scores were examined using multivariable linear regression models.nnRESULTS: Percent DHA at age 8 y was associated with higher reading fluency {β [95% confidence interval (CI)] = 3.54 (0.52, 6.56), P = 0.022} and spelling scores [4.49 (0.02, 8.95); P = 0.021] at age 9 y, and lower PSLE scores [β (95% CI) =-1.43 (-2.68, -0.618); P = 0.025] (indicating better performance) at age 12 y. However, these associations were attenuated after adjusting for an unhealthy dietary pattern. Total n-3 LC-PUFA at age 8 y was associated with higher reading fluency [β (95% CI) =1.55 (0.03, 3.07); P = 0.046] scores at age 9 y, and lower PSLE scores [β (95% CI) =-0.83 (-1.42, -0.24); P = 0.006] at age 12 y. The association with PSLE scores remained significant even after adjusting for healthy or unhealthy dietary patterns [β (95% CI) =-0.68 (-1.29, -0.08); P = 0.028].nnCONCLUSIONS: Higher plasma total n-3 LC-PUFA and DHA were prospectively associated with better academic performance in primary school children, but the relationship with DHA was modulated by an unhealthy dietary pattern. The results suggest that beyond DHA, total n-3 LC-PUFA status plays a significant role in the cognitive development of children.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid41938234,

title = {Distinct Roles of Positive and Negative Maternal Mental Health in Parenting Styles and Child Development},

author = {Michelle Z L Kee and Desiree Y Phua and Helen Y Chen and Yap Seng Chong and Lourdes Mary Daniel and Peter D Gluckman and Birit F P Broekman and Michael J Meaney},

doi = {10.1016/j.jaacop.2025.11.007},

issn = {2949-7329},

year  = {2026},

date = {2026-04-01},

journal = {JAACAP Open},

volume = {4},

number = {2},

pages = {241--253},

abstract = {OBJECTIVE: Maternal mental health significantly impacts child development, yet the role of positive maternal mental health in shaping parenting and child outcomes remains unclear. This study examined how parenting styles mediate the relation between maternal mental health and developmental outcomes in 4- to 4.5-year-old children.nnMETHOD: This study used data from the multiethnic Growing Up in Singapore Towards healthy Outcomes (GUSTO) cohort. A total of 328 mothers, who were recruited from Singapore hospital maternity units between 2009 and 2010, had completed longitudinal postnatal assessments of their mental health and parenting and child measures in English. Maternal mental health and parenting styles were assessed using the Beck Depression Inventory-II, State-Trait Anxiety Inventory, and Parenting Styles and Dimensions Questionnaire. Behavioral problems, school readiness, executive function, and IQ were assessed in children at 4 to 4.5 years old using validated behavioral and cognitive assessments.nnRESULTS: Bifactor modeling revealed 2 distinct maternal mental health factors, general affective symptoms and positive mental health. The general affective symptoms factor was positively associated with permissive and authoritarian parenting ( = 0.27 and 0.29, s < .001), which mediated the relation to child behavioral problems. Positive mental health correlated only with authoritative parenting ( = 0.19,  < .001), which mediated improvements in child executive function, verbal and numeracy abilities, and IQ.nnCONCLUSION: These findings highlight the distinct role of positive maternal mental health in fostering authoritative parenting, which in turn supports child cognitive development. Public health initiatives should prioritize promoting positive maternal mental health to enhance effective parenting and optimize child cognitive outcomes. Future research should consider paternal influences.nnDIVERSITY & INCLUSION STATEMENT: We worked to ensure sex and gender balance in the recruitment of human participants. We worked to ensure race, ethnic, and/or other types of diversity in the recruitment of human participants. We worked to ensure that the study questionnaires were prepared in an inclusive way. Diverse cell lines and/or genomic datasets were not available. One or more of the authors of this paper self-identifies as a member of one or more historically underrepresented racial and/or ethnic groups in science. We actively worked to promote sex and gender balance in our author group.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid41951638,

title = {Astrocyte fatty acid metabolism as a driver of risk for major depressive disorder},

author = {Eamon Fitzgerald and Nicholas O'Toole and Irina Pokhvisneva and Eric J Nestler and Gustavo Turecki and Corina Nagy and Michael J Meaney},

doi = {10.1038/s41467-026-71542-5},

issn = {2041-1723},

year  = {2026},

date = {2026-04-01},

journal = {Nat Commun},

abstract = {Genome-wide association studies (GWAS) have successfully identified genetic loci associated with major depressive disorder (MDD), yet the complex gene networks underpinning this polygenic risk remain largely uncharacterised. Here, we elucidate the neurobiological mechanisms of MDD by analyzing co-expression networks of 94 risk genes in the human prefrontal cortex. By linking these networks to individual symptoms, we identify the FADS1 (fatty acid desaturase 1) network as a central integrator across symptom clusters. We find that the FADS1 network functions primarily in astrocytes to regulate fatty acid metabolism and influence oligodendrocyte-related cell states. Furthermore, we identify FGF2 as a synaptic effector of this pathway and highlight PPARα (peroxisome proliferator-activated receptor alpha) as a putative therapeutic target. These results establish astrocyte fatty acid metabolism as a critical mechanistic contributor to MDD and a promising avenue for treatment.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid41891445,

title = {Maternal mood entropy and children's hippocampal development: Enduring versus transient effects},

author = {Katherine E Jennings and Daniela G Juarez and Jessica P Uy and Jessica L Buthmann and Yap Seng Chong and Peter D Gluckman and Johan G Eriksson and Marielle V Fortier and Helen Chen and Michael J Meaney and Ai Peng Tan and Ian H Gotlib and Jonas G Miller},

doi = {10.1017/S0954579426101291},

issn = {1469-2198},

year  = {2026},

date = {2026-03-01},

journal = {Dev Psychopathol},

pages = {1--14},

abstract = {Recent research suggests that maternal mood entropy, a novel measure of mood dysfunction, is associated with child outcomes. However, the link between maternal mood entropy and children's structural brain development, and how this association may change across childhood, remains unclear. In a longitudinal study with neuroimaging data collected at ages 4.5, 6, 7.5, and 10.5 years ( = 1,498;  = 674 with neuroimaging), we examined whether maternal mood entropy is associated with children's hippocampal and amygdala volumes over time. Mothers reported on negative mood symptoms at several assessments between ages 3 months and 4.5 years. We calculated maternal mood levels as the sum of mood symptoms and computed maternal mood entropy by applying Shannon's entropy to the distributions of mood questionnaire responses. Maternal mood measures were not associated with amygdala volumes; however, mood entropy was directly associated with smaller hippocampal volumes at age 4.5 years and indirectly associated with smaller hippocampal volumes at 10.5 years through rank-order stability over time. These effects were present beyond the effects of socioeconomic status and intracranial volume and were specific to mood entropy, not mood levels. Our findings indicate that patterns of maternal mood are embedded in early childhood brain structure, setting the stage for subsequent neurodevelopment.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid41469287,

title = {Neurobehavioural links from infant screen time to anxiety},

author = {Pei Huang and Shi Yu Chan and Kathy Xinzhuo Zhou and Jasmine Chuah and Aisleen Mariz Arellano Manahan and Evelyn Chung Ning Law and Shefaly Shorey and Helen Juan Zhou and Marielle Valerie Fortier and Yap-Seng Chong and Michael Joseph Meaney and Ai Peng Tan},

doi = {10.1016/j.ebiom.2025.106093},

issn = {2352-3964},

year  = {2026},

date = {2026-01-01},

journal = {EBioMedicine},

volume = {123},

pages = {106093},

abstract = {BACKGROUND: Infant screen time is linked to many negative outcomes, including anxiety, but the underlying neural correlates and pathways remains understudied. We aimed to assess the directional association between infant screen time, development of brain network topology, decision-making behaviour and anxiety symptoms in adolescence.nnMETHODS: Using data from the Growing Up in Singapore Towards healthy Outcomes (GUSTO) cohort study, we examined the effects of total daily screen time for infants on developmental outcomes using structural equation modelling. Specifically, we looked at the developmental slopes of network integration for the seven major brain cortical networks between ages 4.5, 6.0, and 7.5, decision-making behaviour assessed using the Cambridge Gambling Task (CGT) and anxiety symptoms assessed using the Multidimensional Anxiety Scale for Children, 2nd Edition (MASC). This study included 168 children from the GUSTO cohort with data on infant screen time (ages 1-2), diffusion MRI (ages 4.5-7.5), data on decision-making performance (CGT at age 8.5), and anxiety symptoms (MASC at age 13). Brain network integration was derived from diffusion MRI and each participant's developmental slopes were modelled using latent growth models. Structural equation modelling assessed pathways linking early screen time to adolescent anxiety, mediated by brain network development and decision-making.nnFINDINGS: Higher infant screen time was associated with a steeper decline in visual-cognitive control network integration from ages 4.5-7.5 years (β = -1.03 (-1.61, -0.46)), which mediated increased CGT deliberation time at age 8.5. Deliberation time, in turn, was associated with greater anxiety symptoms at age 13. A full serial mediation pathway was significant, linking infant screen time to later anxiety via accelerated brain network maturation and decision-making behaviour (β = 0.033 (0.002, 0.160)).nnINTERPRETATION: Higher infant screen time is linked to accelerated topological maturation of the visual and cognitive control networks, leading to prolonged decision latency and increased adolescent anxiety. Sensory processing impairment may underlie this novel neurodevelopmental pathway, highlighting a potential target for early intervention.nnFUNDING: This research was supported by the Singapore National Research Foundation, Singapore Ministry of Health's National Medical Research Council (NMRC), Singapore, Institute for Human Development and Potential, Agency for Science, Technology and Research, Singapore, the Hope for Depression Research Foundation, USA, the Toxic Stress Network of the JPB Foundation, USA, and the Jacobs Foundation, Switzerland.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid41380478,

title = {Sex-specific interaction effects of Syntaxin 1A coexpression network and childhood trauma on adult depressive symptoms},

author = {Danusa Mar Arcego and Carla Dalmaz and Irina Pokhvisneva and Zihan Wang and Barbara Barth and Sachin Patel and Qizhou Xia and Randriely Merscher Sobreira de Lima and Euclides J de Mendonça Filho and Michael S Kobor and Kieran O'Donnell and Michael J Meaney and Patrícia P Silveira},

doi = {10.1016/j.ebiom.2025.106062},

issn = {2352-3964},

year  = {2026},

date = {2026-01-01},

journal = {EBioMedicine},

volume = {123},

pages = {106062},

abstract = {BACKGROUND: Disruptions in synaptic function and exposure to early life trauma are both implicated in the development of depression, though the underlying mechanisms remain poorly understood.nnMETHODS: To investigate this relationship, we developed an expression-based polygenic score (ePRS) that captures individual variations in the expression of genes co-expressed with the synaptic protein Syntaxin 1A (STX1A) in the prefrontal cortex (PFC). This polygenic score allows us to explore the impact of variations on synaptic function and childhood trauma on the susceptibility to depressive symptoms in adulthood.nnFINDINGS: Our findings indicate that the PFC-ePRS-STX1A score moderates the effects of childhood trauma on the diagnosis of depression in adult females from the UK Biobank (Logistic regression, β = -0.150, p = 0.001, N = 72,812). A similar result was found in an independent cohort (ALSPAC), where PFC-ePRS-STX1A moderated the effects of childhood trauma on depressive symptoms in younger adult females, confirming the sex-specific moderation effect (GEE analysis, ages 22-23, β = -1.063, p = 0.0046, N = 1846). Functional enrichment analysis of the STX1A-coexpressed network revealed key biological processes related to protein synthesis, with 25.8% associated gene products localised to synaptic components at both pre and postsynaptic sites.nnINTERPRETATION: This highlights the critical role of synaptic plasticity function in the PFC in shaping the long-term effects of early trauma on depression. Our methodology and results offer valuable insights into individual vulnerability to depression following early trauma and highlight synaptic function as a potential target for interventions aimed at mitigating depression risk.nnFUNDING: JPB Foundation; Hope for Depression Research Foundation; CAPES; Fonds de recherche du Québec, and CIHR.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid41510815,

title = {Genome-wide methylation patterns associated with chronic stress},

author = {Nicholas O'Toole and Tie-Yuan Zhang and Eamon Fitzgerald and Xianglan Wen and Josie Diorio and Patricia P Silveira and Benoit Labonté and Eric J Nestler and Michael J Meaney},

doi = {10.1080/17501911.2026.2613012},

issn = {1750-192X},

year  = {2026},

date = {2026-01-01},

journal = {Epigenomics},

volume = {18},

number = {1},

pages = {73--88},

abstract = {BACKGROUND: Chronic social defeat stress (CSDS) is a validated animal model for depression that produces sustained behavioral and transcriptional changes in the brain, notably the nucleus accumbens (nAcc).nnRESEARCH DESIGN AND METHODS: We used genome-wide analysis of cytosine methylation patterns in mouse nAcc following CSDS to identify candidate epigenetic mechanisms.nnRESULTS: CSDS produced extensive differential methylation, increasing CG hypermethylation compared to control conditions; non-CG methylation showed the opposite trend. Highly differentially methylated (DM) regions included several genes implicated in behavioral effects of CSDS, including estrogen receptor alpha (Esr1).nnCONCLUSIONS: Analysis of DM sites within gene bodies revealed ß-catenin as a hub gene of a network including the ß-catenin-related WNT/frizzled signaling pathway. Analysis of DM sites upstream of transcription start sites revealed a gene network with the Tcf4 transcription factor as a hub. Genes DM within the gene body were enriched for synaptic function and primarily expressed in D1+ and D2+ medium spiny neurons, which, like the WNT/ß-catenin pathway, are estrogen sensitive and implicated in the behavioral effects of CSDS. We found significant overlap between DM genes associated with CSDS and those associated with major depressive disorder in genome-wide association studies, suggesting that effects on DNA methylation are implicated in the molecular pathways that link chronic stress to depression.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid41401006,

title = {Cognition varies across the calendar year in multiple large-scale datasets},

author = {Arielle S Keller and Alisha Shetty and Ran Barzilay and Monica E Calkins and Yap-Seng Chong and Niyati Dave and Damien A Fair and Peter D Gluckman and Raquel E Gur and Ruben C Gur and Allyson P Mackey and Michael J Meaney and Lucille A Moore and Tyler M Moore and Theodore D Satterthwaite and Ai Peng Tan and Brenden Tervo-Clemmens and Bart S Larsen},

doi = {10.1073/pnas.2506054122},

issn = {1091-6490},

year  = {2025},

date = {2025-12-01},

journal = {Proc Natl Acad Sci U S A},

volume = {122},

number = {51},

pages = {e2506054122},

abstract = {Children's cognitive abilities vary across short and long timescales, from circadian fluctuations to year-by-year developmental changes. "Summer slide" refers to seasonal variation in academic performance, characterized by decreased performance following an extended school vacation. However, it remains unclear whether this effect generalizes across varied assessments and the extent of this effect across sociodemographic groups has been debated. Though seasonal variation in cognitive performance is often attributed to "forgetting" of learned material, no large-scale studies have systematically investigated seasonal variation in general cognitive skills (e.g., executive functioning) on standardized laboratory-based assessments in school-age youth compared to adults. Across four datasets with geographic, demographic, mental health, and measurement variation (total  = 23,251), we quantify cyclical, seasonal variation in children's cognitive performance using generalized additive models with cyclic cubic splines. In school-age children but not young adults, we found consistent cognitive performance minima following school vacation (July-September in the United States; November-January in Singapore) across nearly all cognitive domains investigated. These results demonstrate a generalizable small-magnitude effect of lower cognitive performance aligning with school vacation even after adjusting for socioeconomic status or ADHD diagnosis. We contextualize summer cognitive minima relative to environmental and developmental effects, noting that the largest effect size is still seven times smaller than effects of the socioeconomic environment on cognition, and provide recommendations for future data collection and analysis of behavior across the calendar year.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid41077073,

title = {Feeding practices and concerns as mediators between maternal mental health and eating behaviours in early childhood},

author = {Monica A Lazarus and Beatrice Franzolini and Johan G Eriksson and Mary F-F Chong and Toh Jia Ying and Maria de Iorio and Michael J Meaney and Keith M Godfrey and Fabian Yap and Helen Chen and Yap Seng Chong and Michelle Z L Kee and Anna M Fogel},

doi = {10.1016/j.appet.2025.108340},

issn = {1095-8304},

year  = {2025},

date = {2025-10-01},

journal = {Appetite},

volume = {217},

pages = {108340},

abstract = {BACKGROUND: The impact of maternal mental health on child eating beyond infancy is understudied. This study explores whether maternal feeding practices and concerns mediate the association between maternal depression and anxiety symptoms and eating behaviours at age three years.nnMETHODS: Data from 409 mother-child dyads in the Growing Up in Singapore Towards healthy Outcomes cohort were analysed. Maternal mental health was assessed using the Beck Depression Inventory-II and State-Trait Anxiety Inventory, feeding practices and concerns with the Preschooler Feeding Questionnaire, and child eating behaviours with the Children's Eating Behaviour Questionnaire. Structural equation modelling was used to test pathways.nnRESULTS: Depression symptoms in mothers showed direct and indirect links to child eating behaviours. For example, maternal depression symptoms were directly associated with enjoyment of food (B = 0.011, p = 0.015) and indirectly with food responsiveness (B = 0.004, p = 0.034) via use of food to calm the child. Anxiety symptoms, however, had only indirect associations with child eating behaviours through maternal feeding concerns, not practices. For example, maternal anxiety symptoms were indirectly linked with food responsiveness through perceived difficulty in feeding (B = -0.001, p = 0.011).nnCONCLUSIONS: Depression and anxiety symptoms influence children's eating behaviours differently. Anxiety symptoms were linked with child eating behaviours only through maternal feeding concerns, whereas depression symptoms were linked with child eating behaviours both directly and indirectly via feeding to calm the child. As maternal anxiety symptoms are linked with more child eating concerns, the validity of mother-reported child eating behaviours requires consideration.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid41045207,

title = {Disorders of Arousal in Children and Associated Emotional-Behavioural Problems: Results From a Non-Clinical Longitudinal Cohort},

author = {Christine Laganière and Hélène Gaudreau and Samantha Kenny and Michael Meaney and Marie-Hélène Pennestri},

doi = {10.1111/jsr.70207},

issn = {1365-2869},

year  = {2025},

date = {2025-10-01},

journal = {J Sleep Res},

pages = {e70207},

abstract = {This study aimed to assess the associations between the frequency of episodes of disorders of arousal (sleepwalking and sleep terrors) and emotional-behavioural problems in a longitudinal cohort of healthy children aged 4 and 5 years. Mother-child dyads (N = 345) were recruited during pregnancy for a longitudinal cohort study. Mothers completed validated questionnaires when children were 4 and 5 years old. Linear regressions assessed (1) the concurrent association between the frequency of disorders of arousal episodes (i.e., sleepwalking and sleep terrors) and emotional-behavioural problems in children at 4 and 5; and (2) the association between the frequency of disorders of arousal episodes at 4 and emotional-behavioural problems at 5. Models included the following covariates: child's sex, child's nighttime sleep duration, socioeconomic status and maternal depressive symptoms. More frequent episodes of disorders of arousal at age 4 were significantly associated with more concurrent internalising (B = 2.659, p = 0.001), and externalising problems (B = 2.740, p = 0.006). At age 5, the frequency of episodes was not associated with concurrent internalising and externalising problems (p > 0.05). More frequent episodes at age 4 were associated with more externalising problems at 5 (B = 2.462, p = 0.039). Although sleep terrors and sleepwalking are often benign, our results show that even in a non-clinical cohort, these sleep phenomena can be associated with emotional-behavioural problems in children as young as 4. While the mere presence of sleep terrors or sleepwalking is not alarming, screening for emotional-behavioural problems seems appropriate for children with frequent episodes.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid41168153,

title = {Childhood gut microbiome is linked to internalizing symptoms at school age via the functional connectome},

author = {Francesca R Querdasi and Jessica P Uy and Jennifer S Labus and Jia Xu and Neerja Karnani and Ai Peng Tan and Birit B F P Broekman and Peter D Gluckman and Yap Seng Chong and Helen Chen and Marielle V Fortier and Lourdes Mary Daniel and Fabian Yap and Johan G Eriksson and Shirong Cai and Mary Foong-Fong Chong and Jia Ying Toh and Keith M Godfrey and Michael J Meaney and Bridget L Callaghan},

doi = {10.1038/s41467-025-64988-6},

issn = {2041-1723},

year  = {2025},

date = {2025-10-01},

journal = {Nat Commun},

volume = {16},

number = {1},

pages = {9359},

abstract = {The microbiome-gut-brain-axis plays a critical role in mental health. However, research linking the microbiome to brain function is limited, particularly during development, when tremendous plasticity occurs and many mental health issues, like depression and anxiety, initially manifest. Further complicating attempts to understand interactions between the brain and microbiome is the complex and multidimensional nature of both systems. In the current observational study (N = 55), we use sparse partial least squares to identify linear combinations of brain networks (brain signatures) derived from resting state fMRI scans at age 6 years that maximally covary with internalizing symptoms at age 7.5 years, before identifying microbe abundances (microbial profiles) derived from 16S rRNA sequencing of stool samples at age 2 years that maximally covary with those brain signatures. Finally, we test whether any early microbial profiles are indirectly associated with later internalizing symptoms via the brain signatures, highlighting potential microbial programming effects. We find that microbes in the Clostridiales order and Lachnospiraceae family are associated with internalizing symptoms in middle childhood through connectivity alterations within emotion-related brain networks.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid40957243,

title = {Neural network topology in children's deceptive behaviors: The role of cognitive control and reward processing},

author = {Liwen Yu and Meng Dai and Pei Huang and Birit F P Broekman and Michael Meaney and Yap Seng Chong and Marielle Valerie Fortier and Peipei Setoh and Henning Tiemeier and Ai Peng Tan and Xiao Pan Ding},

doi = {10.1016/j.dcn.2025.101613},

issn = {1878-9307},

year  = {2025},

date = {2025-09-01},

journal = {Dev Cogn Neurosci},

volume = {76},

pages = {101613},

abstract = {The neural mechanisms related to children's deceptive behaviors remain relatively unexplored. This study aims to address this gap by using measures of functional brain network topology, focusing on the cognitive control and reward processing networks that are closely related to children's deceptive behaviors. The study included 113 6-year-old children from the Growing Up in Singapore Towards Healthy Outcomes (GUSTO) project, a birth cohort study. Children participated in the Dart Game designed to assess their tendencies to cheat and lie. During the game, children were required to throw the ball at a long-distance dartboard without supervision, which provided opportunities to cheat by breaking the rules. After the game, children were questioned about whether they had followed the rule, which provided them with opportunities to lie. Resting-state functional magnetic resonance imaging (rs-fMRI) data were collected from all children at the same age during a different visit. We compared three network topology measures (cognitive control network recruitment, reward processing network recruitment and reward-control network integration) between non-cheaters and cheaters, as well as between non-liars and liars. The results showed that a higher degree of cognitive control network recruitment was associated with a greater likelihood of lying. Moreover, a higher degree of reward-cognitive control network integration was associated with a lower likelihood of cheating and lying. The degree of reward processing network recruitment was not associated with deceptive behaviors. These findings help to elucidate how neural mechanisms of cognitive control and reward processing contribute to deceptive behaviors in young children.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid40354717,

title = {Internalizing symptoms and sleep disturbances associated with sleep bruxism in preschoolers},

author = {Christine Laganière and Nelly Huynh and Samantha Kenny and Hélène Gaudreau and Irina Pokhvisneva and Michael Meaney and Marie-Hélène Pennestri},

doi = {10.1016/j.sleep.2025.106553},

issn = {1878-5506},

year  = {2025},

date = {2025-08-01},

journal = {Sleep Med},

volume = {132},

pages = {106553},

abstract = {BACKGROUND AND OBJECTIVES: The presence of sleep bruxism (SB) has been associated with internalizing symptoms and sleep disturbances in school-aged children and adolescents. While manifestations of SB often start earlier in development, there is a lack of studies investigating such an association in younger age groups. Therefore, we assessed the association between SB frequency and (1) internalizing symptoms (anxiety and depression) and (2) sleep disturbances in preschoolers.nnMETHODS: The study comprised 340 mother-child dyads from a longitudinal cohort. Inclusion criteria were full-term pregnancy (>36 weeks), absence of birth complications, absence of severe health issues, and completion of essential measures for the present study. Mothers completed the Children's Sleep Habits Questionnaire when their child was four and five years old. Generalized estimating equation models were used to investigate our main objectives. The models included family socioeconomic status, child's sex, time, child's nighttime sleep duration, and maternal depressive symptoms as covariables.nnRESULTS: More frequent possible SB was associated with more anxiety (B = 0.682, p = 0.009) and depressive symptoms (B = 0.439, p = 0.02) in preschoolers. More frequent possible SB was also associated with more sleep anxiety (B = 0.450, p = 0.002) and bedtime resistance (B = 0.489, p = 0.01) but not with sleep onset delay, sleep duration, and night wakings (p > 0.05).nnCONCLUSIONS: Frequent possible SB episodes in preschoolers may be an indicator of depressive and anxiety difficulties during this developmental period. Bedtime manifestations of internalizing difficulties (bedtime resistance and sleep anxiety) paired with frequent SB in children should warrant further assessment for depressive and anxiety symptoms in preschoolers.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid40290196,

title = {Exposure to Fine Particulate Matter During Pregnancy Is Associated With Hippocampal Development in Offspring},

author = {Jessica L Buthmann and Tarik Benmarhnia and Jonathan Y Huang and Pei Huang and Jonas G Miller and Jessica P Uy and Peter D Gluckman and Marielle V Fortier and Yap-Seng Chong and Ai Peng Tan and Michael J Meaney and Ian H Gotlib},

doi = {10.1016/j.bpsgos.2025.100490},

issn = {2667-1743},

year  = {2025},

date = {2025-07-01},

journal = {Biol Psychiatry Glob Open Sci},

volume = {5},

number = {4},

pages = {100490},

abstract = {BACKGROUND: As the global climate crisis persists, it becomes increasingly important to understand how exposure to environmental toxins can affect the developing brain. Although researchers are beginning to document links between prenatal exposure to air pollution and brain structure, it is not clear when these associations emerge.nnMETHODS: We leveraged data from the GUSTO (Growing Up Toward Healthy Outcomes in Singapore) longitudinal birth cohort study to examine prenatal exposure to air pollution and brain development during childhood. Spatiotemporally interpolated prenatal exposure to particulate matter <2.5 μm was averaged across each prenatal week. Structural magnetic resonance imaging data were obtained when children were ages 4.5, 6.0, 7.5, and 10.5 years ( = 325, 47.7% female) and segmented with FreeSurfer 7.1. A subset of parents completed the Child Behavior Checklist at the final assessment ( = 195, 46.7% female). We used latent growth modeling to estimate a slope of hippocampal volume growth in each hemisphere from ages 4.5 to 10.5 years, adjusted for intracranial volume.nnRESULTS: Distributed lag models indicated that late gestational exposure (during weeks 36-40) was associated with slower hippocampal growth in both hemispheres. Importantly, we also found that faster hippocampal volume growth in the right hemisphere was associated with more externalizing and attention problems at 10.5 years.nnCONCLUSIONS: Future research should examine mechanisms that may underlie or contribute to these associations. These findings underscore the importance of efforts to reduce pollution, particularly for pregnant people and their children.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid40615152,

title = {Universal, selective and indicated parenting interventions to prevent the development of adverse mental health outcomes in youth: a meta-review of systematic reviews},

author = {Meredith X Han and Edward Chesney and Valerie Ng and Joanna Bright and Yashna K Sagar and Ellie Baker and Michael J Meaney and Evelyn C Law},

doi = {10.1136/bmjment-2025-301613},

issn = {2755-9734},

year  = {2025},

date = {2025-07-01},

journal = {BMJ Ment Health},

volume = {28},

number = {1},

abstract = {BACKGROUND: Preventive interventions in the form of parenting support can reduce the risk of mental disorders in children. Summarising the effectiveness of parenting interventions across different levels of prevention can inform the prioritisation of the intervention.nnOBJECTIVES: We conducted a meta-review of systematic reviews and meta-analyses on universal, selective and indicated parenting interventions to prevent adverse mental health outcomes in youth.nnSTUDY SELECTION AND ANALYSIS: PubMed, Ovid, Embase and PsycNet were searched. Systematic reviews consisting of randomised controlled trials of preventative parenting interventions were included. We provided a narrative synthesis of the results and assessed the quantity and quality of evidence for each level of prevention (ie, universal, selective, indicated) and mental health outcome.nnFINDINGS: We identified 32 systematic reviews and meta-analyses, which included 354 randomised controlled trials, consisting of over 74 558 children and adolescents. Universal parenting interventions were effective in delaying the initiation of alcohol and cannabis use, but did not have consistent findings in preventing disruptive behaviour and mood disorders. Selective interventions were predominantly beneficial for disruptive behavioural problems across a variety of risk factors. Indicated interventions found substantial and consistent evidence for reducing problems in children with behavioural problems. Caution is warranted when interpreting findings, as the overall confidence rating of most reviews was very low, especially in the reporting of study selection and justifying exclusions in the AMSTAR-2.nnCONCLUSIONS: Our findings highlight the need for robust evidence synthesis. Despite the limitations of the current evidence base, parenting interventions hold promise for preventing mental health disorders.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid40519638,

title = {Peripheral MicroRNA Signatures in Adolescent Depression},

author = {Alice Morgunova and Nicholas O'Toole and Fatme Abboud and Saché Coury and Gary Gang Chen and Maxime Teixeira and Eamon Fitzgerald and Gustavo Turecki and Anthony J Gifuni and Ian H Gotlib and Corina Nagy and Michael J Meaney and Tiffany C Ho and Cecilia Flores},

doi = {10.1016/j.bpsgos.2025.100505},

issn = {2667-1743},

year  = {2025},

date = {2025-07-01},

journal = {Biol Psychiatry Glob Open Sci},

volume = {5},

number = {4},

pages = {100505},

abstract = {BACKGROUND: Adolescent depression is linked to enduring maladaptive outcomes, chronic severity of symptoms, and poor treatment response. Identifying epigenetic signatures of adolescent depression is urgently needed to improve early prevention and intervention strategies. MicroRNAs (miRNAs) are epigenetic regulators of adolescent neurodevelopmental processes, but their role as markers and mediators of adolescent depression is unknown.nnMETHODS: Here, we examined miRNA profiles from dried blood spot samples of male and female adolescents with clinical depression and psychiatrically healthy male and female adolescents ( = 62). We processed and sequenced these samples using a small RNA protocol tailored for miRNA identification.nnRESULTS: We identified 9 differentially expressed (DE) miRNAs (adjusted  value < .05), all of which were upregulated in adolescents with depression. At future follow-ups post blood collection, expression of miR-3613-5p, mir-30c-2, and miR-942-5p were positively associated with depression severity but not anxiety, suggesting a stronger link to persistent depression symptoms. Expression of miR-32-5p inversely correlated with hippocampal volume, highlighting a potential neurobiological basis. Common predicted gene targets of the DE miRNAs are involved in neurodevelopment, cognitive processing, and depressive disorders.nnCONCLUSIONS: These findings lay the groundwork for identifying adolescent peripheral miRNA markers that reflect neurodevelopmental pathways that shape lifelong psychopathology risk.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}