Inflammation: A Proposed Intermediary Between Maternal Stress and Offspring Neuropsychiatric Risk.

Inflammation: A Proposed Intermediary Between Maternal Stress and Offspring Neuropsychiatric Risk.
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炎症:母亲压力和后代神经精神风险之间的中介因素。

DOI:
10.1016/j.biopsych.2018.08.018
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发表时间:
2019-01-15
影响因子:
10.6
通讯作者:
Epperson CN
Epperson CN
中科院分区:
医学1区
文献类型:
--
作者:
Hantsoo L;Kornfield S;Anguera MC;Epperson CN

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During pregnancy, programming of the fetal central nervous system (CNS) establishes vulnerabilities for emergence of neuropsychiatric phenotypes later in life. Psychosocial influences during pregnancy, such as stressful life events or chronic stress, correlate with offspring neuropsychiatric disorders and with inflammation, respectively. Stress promotes inflammation, but the role of inflammation as a mediator between maternal psychosocial stress and offspring neuropsychiatric outcomes has not been extensively studied in humans. This review summarizes clinical evidence linking specific types of stress to maternal inflammatory load during pregnancy. We propose that inflammation is a mediator in the relationship between psychosocial stress and offspring neuropsychiatric outcomes, potentially influenced by poor maternal glucocorticoid-immune coordination. We present relevant experimental animal research supporting this hypothesis. We conclude that clinical and preclinical research support the premise that stress-induced maternal immune activation (MIA) contributes in part to prenatal programming of risk. Programming of risk is likely due to a combination of vulnerabilities, including multiple or repeated inflammatory events, timing of such events, poor maternal regulation of inflammation, genetic vulnerability, and lifestyle contributors.
DOI: 10.1038/npp.2010.159
发表时间: 2010-12
期刊: Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology
影响因子: --
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