ReviewNeuroscience research2016
Studying longitudinal trajectories in animal models of psychiatric illness and their translation to the human condition.
Review in Neuroscience research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
4 citing papers in PubMed.
- The adipose tissue keeps the score: priming of the adrenal-adipose tissue axis by early life stress predisposes women to obesity and cardiometabolic risk.Frontiers in endocrinology · 2024Review
- Oxytocin-Receptor Gene Modulates Reward-Network Connection and Relationship with Empathy Performance.Psychology research and behavior management · 2023Article
- Four Actionable Bottlenecks and Potential Solutions to Translating Psychiatric Genetics Research: An Expert Review.Public health genomics · 2020Review
- Intrauterine exposure to maternal stress alters Bdnf IV DNA methylation and telomere length in the brain of adult rat offspring.International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
Many forms of psychopathology and/or psychiatric illness can occur through the pathways of altered environmental sensitivity, impulsivity, social functioning, and anxious responding. While these traits are also heritable, environmental conditions are known to play a critical role. The genetic factors that contribute to these traits may be adaptive in certain contexts, but can - under the environmental conditions commonly faced among modern humans - also be key moderators of risk for psychopathological outcomes. This article will discuss how animal studies inform us of the various environmental mechanisms through which prenatal or early postnatal environmental challenge can produce long-term effects on behavior and will briefly address how pre-copulatory, pre-natal and early postnatal epigenetic effects can contribute to persistent alterations in offspring behavior. Its main focus will be how nonhuman primate studies have helped us to understand how genetic vulnerability factors can moderate responses to early environmental factors, suggesting pathways through which early stress might produce long-term effects, thus pointing to systems that might moderate risk for psychiatric illnesses in humans.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.