Background: Fear learning is a core component of conceptual models of how adverse experiences may influence psychopathology. Specifically, existing theories posit that childhood experiences involving childhood trauma are associated with altered fear learning processes, while experiences involving deprivation are not. Several studies have found altered fear acquisition in youth exposed to trauma, but not deprivation, although the specific patterns have varied across studies. The present study utilizes a longitudinal sample of children with variability in adversity experiences to examine associations among childhood trauma, fear learning, and psychopathology in youth.
Methods: The sample includes 170 youths aged 10-13 years ( 11.56, s.d. = 0.47, 48.24% female). Children completed a fear conditioning task while skin conductance responses (SCR) were obtained, which included both acquisition and extinction. Childhood trauma and deprivation severity were measured using both parent and youth report. Symptoms of anxiety, externalizing problems, and post-traumatic stress disorder (PTSD) were assessed at baseline and again two-years later.
Results: Greater trauma-related experiences were associated with greater SCR to the threat cue (CS+) relative to the safety cue (CS-) in early fear acquisition, controlling for deprivation, age, and sex. Deprivation was unrelated to fear learning. Greater SCR to the threat cue during early acquisition was associated with increased PTSD symptoms over time controlling for baseline symptoms and mediated the relationship between trauma and prospective changes in PTSD symptoms.
Conclusions: Childhood trauma is associated with altered fear learning in youth, which may be one mechanism linking exposure to violence with the emergence of PTSD symptoms in adolescence.
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http://dx.doi.org/10.1017/S0033291724001569 | DOI Listing |
Neurosci Biobehav Rev
January 2025
Department of Psychology, University of Turin, Turin, Italy; Department of Medical and Clinical Psychology, Tilburg University, Netherlands; Centro Linceo Interdisciplinare "Beniamino Segre", Accademia Nazionale dei Lincei, Roma, Italy. Electronic address:
Fear responses to novel stimuli can be learned directly, through personal experiences (Fear Conditioning, FC), or indirectly, by observing conspecific reactions to a stimulus (Social Fear Learning, SFL). Although substantial knowledge exists about FC and SFL in humans and other species, they are typically conceived as mechanisms that engage separate neural networks and operate at different levels of complexity. Here, we propose a broader framework that links these two fear learning modes by supporting the view that social signals may act as unconditioned stimuli during SFL.
View Article and Find Full Text PDFPLoS One
January 2025
Department of Obstetrics and Gynecology, Muhimbili University of Health and Allied Sciences, MUHAS, Dar es Salaam, Tanzania.
Background: Despite existing policies promoting companionship, it remains uncommon in Tanzania. Pregnant women select a trusted individual to accompany them during childbirth, providing emotional, physical, and spiritual support. The World Health Organization recommends birth companionship as integral to intrapartum care for positive maternal and fetal outcomes.
View Article and Find Full Text PDFBrain
December 2024
Wellcome Centre for Integrative Neuroimaging, FMRIB, Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford OX3 9DU, UK.
Chronic pain and fatigue in musculoskeletal disease contribute significantly to disability, and recent studies suggest an association with reduced motivation and excessive fear avoidance. In this behavioural neuroimaging study, we aimed to identify the specific behavioral and neural changes associated with musculoskeletal pain and fatigue during reward and loss decision-making. Twenty-nine participants with chronic inflammatory arthritis and 28 healthy controls performed an instrumental learning task (4-armed bandit) during 3T brain fMRI.
View Article and Find Full Text PDFBackground: While the formation of β-amyloid plaques and neurofibrillary "tau" tangles are considered hallmarks of AD pathology, therapeutic targeting of these pathways has been unsuccessful, highlighting the necessity to define the underlying molecular mechanisms driving AD progression. Previous studies from our lab demonstrated that mitochondrial calcium (Ca) overload through neuronal ablation of the mitochondrial Na/Ca exchanger (NCLX) is sufficient to trigger 'AD-like' pathology, including mitochondrial dysfunction, amyloid deposition and tau pathology, and cognitive decline. In addition, we found significant proteomic remodeling of components of the mitochondrial calcium uniporter channel (mtCU), the primary mediator of Ca uptake, in frontal cortex samples isolated post-mortem from patients diagnosed with non-familial/sporadic AD.
View Article and Find Full Text PDFBackground: Previous studies have documented age-related changes in behavior and cognitive functions and investigated the molecular changes in aging brain using inbred mouse strains such as C57BL/6, BALB/c etc. In this study using a genetically heterogenous mouse population (UM-HET3) we investigated age-related changes in motor and memory functions and their association with blood cell measures.
Method: Both male and female UM-HET3 mice at age of 11 months (middle-aged) and 25 months (old) were used in this study.
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