Prenatal Maternal Depression Associates with Microstructure of Right Amygdala in Neonates at Birth

Rifkin‐Graboi, Anne; Bai, Jiaojiao; Chen, Helen; Hameed, Waseem Bak R.; Sim, Lit Wee; Tint, Mya Thway; Leutscher-Broekman, Birit; Chong, Yap Seng; Gluckman, Peter D.; Fortier, Marielle V.; Meaney, Michael J.; Qiu, Anqi

doi:10.1016/j.biopsych.2013.06.019

Cited by 224 publications

(218 citation statements)

References 62 publications

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“…These studies reported delayed overall brain growth, limbic systemspecific volumetric changes, and white matter abnormalities (Li et al, 2012;Lou et al, 1994;Qiu et al, 2013Qiu et al, , 2015Rifkin-Graboi et al, 2013). Such early observations appear to persist into childhood and adolescence, are correlated with affective problems, and may contribute to symptoms in patients with schizophrenia and autism (Buss et al, 2010(Buss et al, , 2012Davis et al, 2013;Du et al, 2013;Sarkar et al, 2014;Zikopoulos and Barbas, 2010).…”

Section: Reprogramming In the Prenatally Stressed Brainmentioning

confidence: 96%

The Placenta as a Mediator of Stress Effects on Neurodevelopmental Reprogramming

Bronson

Bale

2015

Neuropsychopharmacol

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Adversity experienced during gestation is a predictor of lifetime neuropsychiatric disease susceptibility. Specifically, maternal stress during pregnancy predisposes offspring to sex-biased neurodevelopmental disorders, including schizophrenia, attention deficit/hyperactivity disorder, and autism spectrum disorders. Animal models have demonstrated disease-relevant endophenotypes in prenatally stressed offspring and have provided unique insight into potential programmatic mechanisms. The placenta has a critical role in the deleterious and sex-specific effects of maternal stress and other fetal exposures on the developing brain. Stress-induced perturbations of the maternal milieu are conveyed to the embryo via the placenta, the maternal-fetal intermediary responsible for maintaining intrauterine homeostasis. Disruption of vital placental functions can have a significant impact on fetal development, including the brain, outcomes that are largely sex-specific. Here we review the novel involvement of the placenta in the transmission of the maternal adverse environment and effects on the developing brain.

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Section: Reprogramming In the Prenatally Stressed Brainmentioning

confidence: 96%

The Placenta as a Mediator of Stress Effects on Neurodevelopmental Reprogramming

Bronson

Bale

2015

Neuropsychopharmacol

205

180

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“…In support of this idea, postnatal maternal mood, controlling for prenatal mood, predicts hippocampal growth trajectories (11). Similarly, prenatal maternal cortisol levels associate with the amygdala but not hippocampus volume in middle childhood (10). The reasons for regional specificity are not obvious and unlikely to map readily onto normal developmental profiles.…”

Section: Sensitive Periodsmentioning

confidence: 98%

“…For example, the authors note that Lupien et al (3) reported MRI findings with similarly aged subjects (mid-childhood), showing an association between postnatal maternal depression and the volume of the amygdala, but not the hippocampus. However, there are prenatal maternal influences, including maternal mood on the amygdala but not hippocampal volume, which are sustained into late childhood (9,10). Because maternal mood generally remains stable across the peripartum period, the Lupien et al (3) findings might reflect a prenatal maternal mood, thus resolving the apparent contradiction.…”

Section: Sensitive Periodsmentioning

confidence: 99%

Mother nurture and the social definition of neurodevelopment

Meaney

2016

Proc. Natl. Acad. Sci. U.S.A.

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“…Since the amygdala is involved in emotional processing, these children may have greater vulnerability to emotional problems. Lower amygdala FA was also found in infants whose mothers had greater prenatal depressive symptoms 35 ; hence, future studies should include maternal depressive symptoms as a covariate to determine whether these symptoms might account for the lower amygdala FA in younger e2e3 children.…”

Section: Brain Regions With Apoe E-by-age Interactions Are Shown (Grementioning

confidence: 99%

Gray matter maturation and cognition in children with different APOE ε genotypes

et al. 2016

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Objective: The aims of the current study were to determine whether children with the 6 different APOE e genotypes show differences in gray matter maturation, particularly for those with e4 and e2 alleles, which are associated with poorer outcomes in many neurologic disorders.Methods: A total of 1,187 healthy children (aged 3-20 years, 52.1% boys, 47.9% girls) with acceptable data from the cross-sectional Pediatric Imaging Neurocognition and Genetics Study were evaluated for the effects of 6 APOE e genotypes on macroscopic and microscopic cortical and subcortical gray matter structures (measured with 3-tesla MRI and FreeSurfer for automated morphometry) and on cognition (NIH Toolbox).Results: Among APOE e4 carriers, age-related changes in brain structures and cognition varied depending on genotype, with the smallest hippocampi in e2e4 children, the lowest hippocampal fractional anisotropy in younger e4e4 children, the largest medial orbitofrontal cortical areas in e3e4 children, and age-dependent thinning of the entorhinal cortex in e4e4 children. Younger e4e4 children had the lowest scores on executive function and working memory, while younger e2e4 children performed worse on attention tasks. Larger parietal gyri in the younger e2e4 children, and thinner temporal and cingulate isthmus cortices or smaller hippocampi in the younger e4e4 children, predicted poorer performance on attention or working memory.Conclusions: Our findings validated and extended prior smaller studies that showed altered brain development in APOE e4-carrier children. The e4e4 and e2e4 genotypes may negatively influence brain development and brain aging at the extremes of age. Studying APOE e polymorphisms in young children may provide the earliest indicators for individuals who might benefit from early interventions or preventive measures for future brain injuries and dementia. Neurology ® 2016;87:585-594 GLOSSARY AD 5 Alzheimer disease; FA 5 fractional anisotropy; GAF 5 genetic ancestry factor; GAM 5 general additive model; PING 5 Pediatric Imaging, Neurocognition, and Genetics; ROI 5 region of interest; SES 5 socioeconomic status; WM 5 working memory.

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Prenatal Maternal Depression Associates with Microstructure of Right Amygdala in Neonates at Birth

Cited by 224 publications

References 62 publications

The Placenta as a Mediator of Stress Effects on Neurodevelopmental Reprogramming

The Placenta as a Mediator of Stress Effects on Neurodevelopmental Reprogramming

Mother nurture and the social definition of neurodevelopment

Gray matter maturation and cognition in children with different APOE ε genotypes

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