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J Neurosci. 2017 Nov 8;37(45):10783-10791. doi: 10.1523/JNEUROSCI.1822-17.2017.

Social Origins of Developmental Risk for Mental and Physical Illness.

Author information

1
Department of Psychiatry, University of Pittsburgh, Pittsburgh, Pennsylvania 15213, jcameron@pitt.edu.
2
Department of Pediatrics, Keck School of Medicine, University of Southern California, Children's Hospital Los Angeles, Los Angeles, California 90027.
3
Department of Human Development and Quantitative Methodology, University of Maryland, College Park, Maryland 20742.
4
Center for Brain Science, Department of Molecular Cellular Biology, Harvard University, Cambridge, Massachusetts 02138, and.
5
F. M. Kirby Neurobiology Center, Department of Neurology, Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts 02115.

Abstract

Adversity in early childhood exerts an enduring impact on mental and physical health, academic achievement, lifetime productivity, and the probability of interfacing with the criminal justice system. More science is needed to understand how the brain is affected by early life stress (ELS), which produces excessive activation of stress response systems broadly throughout the child's body (toxic stress). Our research examines the importance of sex, timing and type of stress exposure, and critical periods for intervention in various brain systems across species. Neglect (the absence of sensitive and responsive caregiving) or disrupted interaction with offspring induces robust, lasting consequences in mice, monkeys, and humans. Complementary assessment of internalizing disorders and brain imaging in children suggests that early adversity can interfere with white matter development in key brain regions, which may increase risk for emotional difficulties in the long term. Neural circuits that are most plastic during ELS exposure in monkeys sustain the greatest change in gene expression, offering a mechanism whereby stress timing might lead to markedly different long-term behaviors. Rodent models reveal that disrupted maternal-infant interactions yield metabolic and behavioral outcomes often differing by sex. Moreover, ELS may further accelerate or delay critical periods of development, which reflect GABA circuit maturation, BDNF, and circadian Clock genes. Such factors are associated with several mental disorders and may contribute to a premature closure of plastic windows for intervention following ELS. Together, complementary cross-species studies are elucidating principles of adaptation to adversity in early childhood with molecular, cellular, and whole organism resolution.

KEYWORDS:

EEG; foster care; limbic; neglect; parvalbumin; sex-dependent

PMID:
29118206
PMCID:
PMC5678010
DOI:
10.1523/JNEUROSCI.1822-17.2017
[Indexed for MEDLINE]
Free PMC Article

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