Anticipating future threats: Evidence for association, but not interaction, of childhood adversity and identity development with threat anticipation in adolescence.

AIM: Childhood adversity may result in a negative expectation of future interactions with others, also referred to as 'threat anticipation'. It may also negatively impact on identity development, which subsequently may influence how individuals deal with their environment. Here, we examine the hypotheses that (1) identity synthesis is associated with reduced anticipation of threat, whereas the opposite would be true for identity confusion, and (2) that identity confusion exacerbates the association between childhood adversity and threat anticipation. METHODS: One thousand nine hundred and thirteen adolescents from the general population (mean age = 13.8 years, SD = 1.86, range = 11-20) completed self-report questionnaires assessing exposure to childhood adversity, identity development and threat anticipation. RESULTS AND DISCUSSION: Identity development was significantly associated with threat anticipation in the expected direction: identity synthesis was associated with reduced anticipation of threat (ß = -.0013, p < .001), whereas identity confusion was association with increased threat anticipation (ß = .0017, p < .001). Furthermore, childhood adversity was positively associated with threat anticipation (ß = .0018, p < .001). However, no evidence for an interaction effect of identity on the association between childhood adversity and threat anticipation was found, suggesting childhood adversity and identity development have an independent rather than synergistic effect on threat anticipation. CONCLUSION: The current study illustrates the importance of exposure to childhood adversity and identity development for threat anticipation in adolescence. Further research is needed to clarify how both factors influence each other within a developmental framework.

The role of identity in the development of depressive, anxiety, and psychosis symptoms in adolescents exposed to childhood adversity.

INTRODUCTION: Childhood adversity is a major risk factor for psychiatric disorders and has especially been associated with an admixture of depressive, anxiety, and psychosis symptoms. Identity formation, a main developmental task during adolescence, may be impacted by these adverse experiences and act as an important process in the association between childhood adversity and psychopathology. METHODS: We investigated the association between childhood adversity, identity formation, and depressive, anxiety, and psychosis symptoms cross-sectionally in 1913 Flemish adolescents between 11 and 20 years old (mean = 13.76, SD = 1.86). Adolescents completed questionnaires during the first wave of the SIGMA study between January 2018 and May 2019. RESULTS: Childhood interpersonal adversity was associated with increased identity confusion and decreased identity synthesis. Additionally, identity confusion was associated with increased self-reported levels of psychopathology and potentially mediated the association between childhood adversity and psychopathology. CONCLUSION: This study highlights the importance of promoting healthy identity formation in adolescents with and without exposure to adverse childhood experiences.

Exercise to spot the differences: a framework for the effect of exercise on hippocampal pattern separation in humans.

Exercise has a beneficial effect on mental health and cognitive functioning, but the exact underlying mechanisms remain largely unknown. In this review, we focus on the effect of exercise on hippocampal pattern separation, which is a key component of episodic memory. Research has associated exercise with improvements in pattern separation. We propose an integrated framework mechanistically explaining this relationship. The framework is divided into three pathways, describing the pro-neuroplastic, anti-inflammatory and hormonal effects of exercise. The pathways are heavily intertwined and may result in functional and structural changes in the hippocampus. These changes can ultimately affect pattern separation through direct and indirect connections. The proposed framework might guide future research on the effect of exercise on pattern separation in the hippocampus.

Facial Expression Processing Across the Autism-Psychosis Spectra: A Review of Neural Findings and Associations With Adverse Childhood Events.

Autism spectrum disorder (ASD) and primary psychosis are classified as distinct neurodevelopmental disorders, yet they display overlapping epidemiological, environmental, and genetic components as well as endophenotypic similarities. For instance, both disorders are characterized by impairments in facial expression processing, a crucial skill for effective social communication, and both disorders display an increased prevalence of adverse childhood events (ACE). This narrative review provides a brief summary of findings from neuroimaging studies investigating facial expression processing in ASD and primary psychosis with a focus on the commonalities and differences between these disorders. Individuals with ASD and primary psychosis activate the same brain regions as healthy controls during facial expression processing, albeit to a different extent. Overall, both groups display altered activation in the fusiform gyrus and amygdala as well as altered connectivity among the broader face processing network, probably indicating reduced facial expression processing abilities. Furthermore, delayed or reduced N170 responses have been reported in ASD and primary psychosis, but the significance of these findings is questioned, and alternative frequency-tagging electroencephalography (EEG) measures are currently explored to capture facial expression processing impairments more selectively. Face perception is an innate process, but it is also guided by visual learning and social experiences. Extreme environmental factors, such as adverse childhood events, can disrupt normative development and alter facial expression processing. ACE are hypothesized to induce altered neural facial expression processing, in particular a hyperactive amygdala response toward negative expressions. Future studies should account for the comorbidity among ASD, primary psychosis, and ACE when assessing facial expression processing in these clinical groups, as it may explain some of the inconsistencies and confound reported in the field.

Individual differences in processing orientation and proximity as emergent features.

Numerous examples of meaningful inter-individual differences in visual processing have been documented in low- and high-level vision. For mid-level vision or perceptual organization, vision scientists have only recently started to study the inter-individual differences structure. In this study, we focus on orientation and proximity as emergent features and combine a quantitative information processing approach with an individual differences approach. We first replicated the results reported in Hawkins, Houpt, Eidels, and Townsend (2016) in a set of 52 observers. That is, observers showed higher processing capacity for detecting a change in a stimulus configuration when the emergent features orientation or proximity were changed. Next, we asked whether individual differences processing capacities were similar across emergent features. The capacity to detect any type of change correlated moderately across individuals, whereas the capacity to detect changes in either emergent feature alone was not strongly correlated. This indicates that there is no general sensitivity to emergent features and that observers can be good at detecting orientation changes whilst being poor at detecting proximity changes (and vice versa). An additional exploratory multivariate analysis of the data revealed that response times and accuracies correlated strongly within each emergent feature. Moreover, specific factors related to change detection and inward displacements were observed, revealing consistent individual differences in our data. We discuss the results in the context of the literature on individual differences in vision where both specific, fragmented factors as well as broad, general factors have been reported.

Early Cognitive and Behavioral Deficits in Mouse Models for Tauopathy and Alzheimer's Disease.

Neurocognitive disorders, among which Alzheimer's disease (AD), have become one of the major causes of death in developed countries. No effective disease-modifying therapy is available, possibly because current treatments are administered too late to still be able to intervene in the disease progress. AD is characterized by a gradual onset with subclinical neurobiological and behavioral changes that precede diagnosis with years to even decades. The earlier the diagnosis, the earlier potential treatments can be tested and started. Mouse models are valuable to study the possible causes underlying early phases of neuropathology and their reflection in behavior and other biomarkers, to help improve preclinical detection and diagnosis of AD. Here, we assessed cognitive functioning and social behavior in transgenic mice expressing tau pathology only (Tau-P301L) or a combination of amyloid and tau pathology [amyloid precursor protein (APP)-V717I × Tau-P301L]. The mice were subjected to a variety of behavioral tasks at an age of 3-6 months, i.e., at an early phase of their AD-like pathology. We hypothesized that compared to age-matched wild-type controls, transgenic mice would show specific impairments in both cognitive and non-cognitive tasks. In line with our expectations, transgenic mice showed decreased cognitive flexibility in the Morris water maze, decreased exploratory behavior, decreased performance in a nesting task, and increased anxiety-like behavior. In accordance with the amyloid-cascade hypothesis, some of the behavioral measures showed more severe deficits in APP-V717I × Tau-P301L compared to Tau-P301L mice, indicating an exacerbation of disease processes due to the co-occurrence of amyloid and tau pathology. Our study supports the use of behavioral markers as early indicators of ongoing AD pathology during the preclinical phase.