Early child adversity and psychopathology in adulthood: HPA axis and cognitive dysregulations as potential mechanisms

Raymond, Catherine; Marin, Marie‐France; Majeur, Danie; Lupien, Sonia J.

doi:10.1016/j.pnpbp.2017.07.015

Cited by 87 publications

(82 citation statements)

References 104 publications

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“…It is now recognized that such trauma makes persons more vulnerable to stress for the rest of their lives. Stress increases levels of circulating cortisol, and high levels of cortisol have a deleterious effect on the developing brain, particularly on the hippocampus and amygdala . Such effects will also depend on genetic differences and epigenetic changes of specific genes induced by the cortisol.…”

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confidence: 91%

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Functional movement disorders: Is the crisis resolved?

Hallett

2019

Movement Disorders

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confidence: 91%

“…Stress increases levels of circulating cortisol, and high levels of cortisol have a deleterious effect on the developing brain, particularly on the hippocampus and amygdala. 12 Such effects will also depend on genetic differences and epigenetic changes of specific genes induced by the cortisol. A hint of a possible epigenetic change has already been found.…”

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confidence: 99%

Functional movement disorders: Is the crisis resolved?

Hallett

2019

Movement Disorders

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“…Predisposition to cognitive disorders throughout life is established through an interplay of inherited and environmental factors (Caspi et al, 2003;Klengel & Binder, 2015). Brain development during the early postnatal period is particularly susceptible to environmental influences (Brown, Susser, Lin, Neugebauer, & Gorman, 1995;Chen & Baram, 2016;Eriksson, Räikkönen, & Eriksson, 2014;Lupien, McEwen, Gunnar, & Heim, 2009;Novick et al, 2018;Raymond, Marin, Majeur, & Lupien, 2018). In humans, an impoverished environment during childhood is associated with impaired cognition later in life, and an increased risk of dementia (Kaplan et al, 2001;Nelson et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

Short-term block of CRH receptor in adults mitigates age-related memory impairments provoked by early-life adversity

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Maras

Pham³

et al. 2019

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In humans, early-life adversity (ELA) is associated with impairments in learning and memory that may emerge later in life. In rodent models, ELA directly impacts hippocampal neuron structure and connectivity with progressive deficits in long-term potentiation and spatial memory function. Previous work has demonstrated that augmented release and actions of the stressactivated neuropeptide, CRH, contribute to the deleterious effects of ELA on hippocampal structure and memory-function. Early-life adversity increases CRH production and levels, and blocking CRH receptor type 1 (CRHR1) within the hippocampus immediately following adversity prevented the memory and LTP problems caused by ELA. Here we queried if blocking CRHR1 during adulthood ameliorates the adverse impact of ELA on memory in middle age. Blocking CRHR1 for a week in two month old male rats prevented ELA-induced deficits in object recognition memory that emerge during middle age. The intervention failed to mitigate the reduction of spatial memory at 4 and 8 months, but restored hippocampus-dependent location memory in ELA-experiencing rats during middle age (12 months of age).Notably, neither ELA nor blocking CRHR1 influenced anxiety-or depression-related behaviors These findings suggest a sensitive period during which interventions can fully prevent longlasting effects of ELA, yet indicate that interventions later in life offer significant benefits.

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“…Indeed, early-life experiences in themselves seem to play an important role in influencing cognitive outcomes 6,7 . The idea that early-life adversity influences cognitive and emotional health and disease throughout life is supported by strong epidemiological evidence, and the statistical relationship between earlylife adversity and a variety of psychiatric disorders has been extensively documented and reviewed [8][9][10][11][12][13] . While acknowledging the frequent overlap between cognitive and emotional deficits 14 , in this Review we focus primarily on how early-life adversity could modulate cognitive functions across the lifespan, including memory problems in children 10,15,16 , cognitive decline during middle age [17][18][19][20][21][22] , and late-life dementia 17,18,23 .…”

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confidence: 99%

Early-life adversity and neurological disease: age-old questions and novel answers

2019

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Neurological illnesses, including cognitive impairment, memory decline and dementia, affect over 50 million people worldwide, imposing a substantial burden on individuals and society. These disorders arise from a combination of genetic, environmental and experiential factors, with the latter two factors having the greatest impact during sensitive periods in development. In this Review , we focus on the contribution of adverse early-life experiences to aberrant brain maturation, which might underlie vulnerability to cognitive brain disorders. Specifically , we draw on recent robust discoveries from diverse disciplines, encompassing human studies and experimental models. These discoveries suggest that early-life adversity , especially in the perinatal period, influences the maturation of brain circuits involved in cognition. Importantly , new findings suggest that fragmented and unpredictable environmental and parental signals comprise a novel potent type of adversity , which contributes to subsequent vulnerabilities to cognitive illnesses via mechanisms involving disordered maturation of brain 'wiring'.

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Early child adversity and psychopathology in adulthood: HPA axis and cognitive dysregulations as potential mechanisms

Cited by 87 publications

References 104 publications

Functional movement disorders: Is the crisis resolved?

Functional movement disorders: Is the crisis resolved?

Short-term block of CRH receptor in adults mitigates age-related memory impairments provoked by early-life adversity

Early-life adversity and neurological disease: age-old questions and novel answers

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