Acquisition, extinction, and return of fear in veterans in intensive outpatient prolonged exposure therapy: A fear-potentiated startle study.

Prolonged exposure (PE) therapy is a first-line treatment for posttraumatic stress disorder (PTSD) and involves repeated presentation of trauma-related cues without aversive outcomes. A primary learning mechanism of PE is fear extinction (new learning that a dangerous cue is now safe) and its retention (maintaining this new learning over time). Extant research suggests extinction is impaired in PTSD patients.

Micro Versus Macro Processes: How specific stress exposure impacts sleep, affect, and risk-related behavior on the path to disease in high-risk adults.

Background: The stress-to-disease association has been well-accepted for some time. However, the understanding of stress exposure contributes to psychological disease progression remains unclear.

Objective: To test the real-time impact of variable stress exposure on risk-related clinical phenomena and affective disease progression in a high-risk sample of active-duty firefighters.

Predicting negative affect variability and spontaneous emotion regulation: Can working memory span tasks estimate emotion regulatory capacity?

[Correction Notice: An Erratum for this article was reported online in on Jan 7 2021 (see record 2021-06077-001). In the article, in the Results and Discussion sections for Study 2 and in Table 6, it was stated that RSPAN scores predicted spontaneous down-regulation of negative affect from one diary signal to the next. However, because RSPAN scores are a person-level variable, it is an error to describe the results in that way.

A film set for the elicitation of emotion in research: A comprehensive catalog derived from four decades of investigation.

Emotions are highly influential to many psychological processes. Indeed, research employing emotional stimuli is rapidly escalating across the field of psychology. However, challenges remain regarding discrete evocation of frequently co-elicited emotions such as amusement and happiness, or anger and disgust.

A Novel Interaction between Tryptophan Hydroxylase 2 (TPH2) Gene Polymorphism (rs4570625) and BDNF Val66Met Predicts a High-Risk Emotional Phenotype in Healthy Subjects.

Poor inhibitory processing of negative emotional content is central to many psychiatric disorders, including depression and anxiety. Moreover, increasing evidence suggests that core aspects of emotion-inhibitory processing are largely inherited and as such may represent a key intermediate or risk-related phenotype for common affective diseases (e.g.

The transcriptional landscape of age in human peripheral blood.

Disease incidences increase with age, but the molecular characteristics of ageing that lead to increased disease susceptibility remain inadequately understood. Here we perform a whole-blood gene expression meta-analysis in 14,983 individuals of European ancestry (including replication) and identify 1,497 genes that are differentially expressed with chronological age. The age-associated genes do not harbor more age-associated CpG-methylation sites than other genes, but are instead enriched for the presence of potentially functional CpG-methylation sites in enhancer and insulator regions that associate with both chronological age and gene expression levels.

An angiotensin-converting enzyme (ACE) polymorphism may mitigate the effects of angiotensin-pathway medications on posttraumatic stress symptoms.

Angiotensin, which regulates blood pressure may also act within the brain to mediate stress and fear responses. Common antihypertensive medication classes of angiotensin-converting enzyme inhibitors (ACE-Is) and angiotensin receptor blockers (ARBs) have been associated with lower PTSD symptoms. Here we examine the rs4311 SNP in the ACE gene, previously implicated in panic attacks, in the relationship between ACE-I/ARB medications and PTSD symptoms.

Development of fear acquisition and extinction in children: effects of age and anxiety.

Development of anxiety disorders is associated with neurobiological changes in areas that are a critical part of the fear neurocircuitry. Fear conditioning paradigms can offer insight into the mechanisms underlying the neurobiological ontogeny of anxiety. A small number of studies have focused on the effects of age and anxiety separately in school age children.

Translational neuroscience measures of fear conditioning across development: applications to high-risk children and adolescents.

Several mental illnesses, including anxiety, can manifest during development, with onsets in late childhood. Understanding the neurobiological underpinnings of risk for anxiety is of crucial importance for early prevention and intervention approaches. Translational neuroscience offers tools to investigate such mechanisms in human and animal models.