ArticleFrontiers in cellular neuroscience2017
Late-Onset Cognitive Impairments after Early-Life Stress Are Shaped by Inherited Differences in Stress Reactivity.
Article in Frontiers in cellular neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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Who cites it
7 citing papers in PubMed, 18 citations in OpenAlex.
- Early-life adversity in rodents: Experimental design is of the essence.Neurobiology of stress · 2026Article
- Intermittent Fasting and Emotional Regulation: A Psychobiological Framework Integrating Metabolic, Neuroendocrine and Interoceptive Mechanisms.Nutrients · 2026Review
- Early-life stress lastingly impacts microglial transcriptome and function under basal and immune-challenged conditions.Translational psychiatry · 2022Article
- Experience and activity-dependent control of glucocorticoid receptors during the stress response in large-scale brain networks.Stress (Amsterdam, Netherlands) · 2021Article
- Effects ofBrain sciences · 2019Article
- Sex-Dependent Modulation of Acute Stress Reactivity After Early Life Stress in Mice: Relevance of Mineralocorticoid Receptor Expression.Frontiers in behavioral neuroscience · 2019Article
- Social Origins of Developmental Risk for Mental and Physical Illness.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Early-life stress (ELS) has been associated with lasting cognitive impairments and with an increased risk for affective disorders. A dysregulation of the hypothalamus-pituitary-adrenal (HPA) axis, the body's main stress response system, is critically involved in mediating these long-term consequences of adverse early-life experience. It remains unclear to what extent an inherited predisposition for HPA axis sensitivity or resilience influences the relationship between ELS and cognitive impairments, and which neuroendocrine and molecular mechanisms may be involved. To investigate this, we exposed animals of the stress reactivity mouse model, consisting of three independent lines selectively bred for high (HR), intermediate (IR), or low (LR) HPA axis reactivity to a stressor, to ELS and assessed their cognitive performance, neuroendocrine function and hippocampal gene expression in early and in late adulthood. Our results show that HR animals that were exposed to ELS exhibited an HPA axis hyper-reactivity in early and late adulthood, associated with cognitive impairments in hippocampus-dependent tasks, as well as molecular changes in transcript levels involved in the regulation of HPA axis activity (
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.