Prenatal developmental origins of behavior and mental health: The influence of maternal stress in pregnancy

Neuroscience & Biobehavioral Reviews, Год журнала: 2017, Номер 117, С. 26 - 64

Опубликована: Июль 28, 2017

Язык: Английский

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Holocaust Exposure Induced Intergenerational Effects on FKBP5 Methylation

Biological Psychiatry, Год журнала: 2015, Номер 80(5), С. 372 - 380

Опубликована: Авг. 12, 2015

Язык: Английский

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Sex differences and stress across the lifespan

Nature Neuroscience, Год журнала: 2015, Номер 18(10), С. 1413 - 1420

Опубликована: Сен. 25, 2015

Язык: Английский

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Transgenerational Epigenetic Inheritance

Annual Review of Genetics, Год журнала: 2018, Номер 52(1), С. 21 - 41

Опубликована: Авг. 30, 2018

Inheritance of genomic DNA underlies the vast majority biological inheritance, yet it has been clear for decades that additional epigenetic information can be passed on to future generations. Here, we review major model systems transgenerational inheritance via germline in multicellular organisms. In addition surveying examples epivariation may arise stochastically or response unknown stimuli, also discuss induction heritable changes by genetic environmental perturbations. Mechanistically, increasingly well-understood molecular pathways responsible with a focus unusual features epigenome.

Язык: Английский

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Sex differences in the neuro-immune consequences of stress: Focus on depression and anxiety

Brain Behavior and Immunity, Год журнала: 2017, Номер 67, С. 1 - 12

Опубликована: Фев. 17, 2017

Язык: Английский

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Distress During Pregnancy: Epigenetic Regulation of Placenta Glucocorticoid-Related Genes and Fetal Neurobehavior

American Journal of Psychiatry, Год журнала: 2016, Номер 173(7), С. 705 - 713

Опубликована: Март 25, 2016

Objective: Increased risk of psychopathology is observed in children exposed to maternal prenatal distress, and elevated cortisol epigenetic regulation placental glucocorticoid-pathway genes are potential mechanisms. The authors examined distress salivary relation fetal movement heart rate (“coupling”) DNA methylation three glucocorticoid pathway genes—HSD11B2, NR3C1, FKBP5—in term placentas. Method: Mood questionnaires were collected from 61 women between 24–27 gestational weeks, assessment was conducted at 34–37 weeks. Placental CpG the analyzed using 450K Beadchips bisulfite sequencing; correlations variables tested; effects on behavior via investigated. Results: Perceived stress (Perceived Stress Scale), but not cortisol, associated with altered In highest tertile Scale, Beadchip data revealed modestly HSD11B2, lower coupling (β=−0.51), FKBP5, also (β=−0.47). These increases validated by sequencing, where they occurred a minority clones. Conclusions: This first study link pregnant women's fetus changes genes. Since increased HSD11B2 FKBP5 seen sequencing clones, these changes, functional consequences, may affect subpopulations cells.

Язык: Английский

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The future of rodent models in depression research

Nature reviews. Neuroscience, Год журнала: 2019, Номер 20(11), С. 686 - 701

Опубликована: Окт. 2, 2019

Язык: Английский

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The Placenta as a Mediator of Stress Effects on Neurodevelopmental Reprogramming

Neuropsychopharmacology, Год журнала: 2015, Номер 41(1), С. 207 - 218

Опубликована: Авг. 7, 2015

Язык: Английский

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Brain changes in a maternal immune activation model of neurodevelopmental brain disorders

Progress in Neurobiology, Год журнала: 2018, Номер 175, С. 1 - 19

Опубликована: Дек. 24, 2018

The developing brain is sensitive to a variety of insults. Epidemiological studies have identified prenatal exposure infection as risk factor for range neurological disorders, including autism spectrum disorder and schizophrenia. Animal models corroborate this association been used probe the contribution gene-environment interactions etiology neurodevelopmental disorders. Here we review behavior phenotypes that characterized in MIA offspring, looked at interaction between maternal immune activation genetic factors or These include behaviors relevant autism, schizophrenia, other alterations anatomy, structural functional neuronal impairments. link these phenotypic changes not fully understood, but there increasing evidence induces prolonged offspring's which could underlie epigenetic turn may mediate changes. concepts will be discussed followed by summary pharmacological interventions tested model.

Язык: Английский

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Neuro-toxic and Reproductive Effects of BPA

Current Neuropharmacology, Год журнала: 2019, Номер 17(12), С. 1109 - 1132

Опубликована: Июль 30, 2019

Bisphenol A (BPA) is one of the highest volume chemicals produced worldwide. It has recognized activity as an endocrine-disrupting chemical and suspected roles a neurological reproductive toxicant. interferes in steroid signaling, induces oxidative stress, affects gene expression epigenetically. Gestational, perinatal neonatal exposures to BPA affect developmental processes, including brain development gametogenesis, with consequences on functions, behavior, fertility.This review critically analyzes recent findings neuro-toxic effects (and its analogues), focus neuronal differentiation, synaptic plasticity, glia microglia activity, cognitive central local control reproduction.BPA potential human health hazard associated gestational, peri- exposure. Beginning BPA's disposition, this summarizes neurotoxicity analogues, neuroinflammation, neuro-degeneration, impairment abilities. Furthermore, it reports along HPG axis, hypothalamic Gonadotropin Releasing Hormone (GnRH), reproduction both sexes successful pregnancy.BPA analogues impair axis function, reproduction, fertility. Contrasting results have emerged animal models human. Thus, further studies are needed better define their safety levels. This offers new insights these issues aim find "fil rouge", if any, that characterize mechanism action outcomes function reproduction.

Язык: Английский

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