Enhanced emotion regulation capacity and its neural substrates in those exposed to moderate childhood adversity.

Individuals exposed to childhood adversities (CA) present with emotion regulation (ER) difficulties in later life, which have been identified as risk and maintenance factors for psychopathologies. However, it is unclear if CA negatively impacts on ER capacity per se or whether observed regulation difficulties are a function of the challenging circumstances in which ER is being deployed. In this longitudinal study, we aimed to clarify this association by investigating the behavioral and neural effects of exposure to common moderate CA (mCA) on a laboratory measure of ER capacity in late adolescence/young adulthood. Our population-derived samples of adolescents/young adults (N = 53) were administered a film-based ER-task during functional magnetic resonance imaging that allowed evaluation of ER across mCA-exposure. mCA-exposure was associated with enhanced ER capacity over both positive and negative affect. At the neural level, the better ER of negative material in those exposed to mCA was associated with reduced recruitment of ER-related brain regions, including the prefrontal cortex and temporal gyrus. In addition mCA-exposure was associated with a greater down-regulation of the amygdala during ER of negative material. The implications of these findings for our understanding of the effects of mCA on the emergence of resilience in adolescence are discussed

Mood and neural responses to social rejection do not seem to be altered in resilient adolescents with a history of adversity.

Childhood adversity (CA) increases the risk of subsequent mental health problems. Adolescent social support (from family and/or friends) reduces the risk of mental health problems after CA. However, the mechanisms of this effect remain unclear, and we speculate that they are manifested on neurodevelopmental levels. Therefore, we investigated whether family and/or friendship support at ages 14 and 17 function as intermediate variables for the relationship between CA before age 11 and affective or neural responses to social rejection feedback at age 18. We studied 55 adolescents with normative mental health at age 18 (26 with CA and therefore considered "resilient"), from a longitudinal cohort. Participants underwent a Social Feedback Task in the magnetic resonance imaging scanner. Social rejection feedback activated the dorsal anterior cingulate cortex and the left anterior insula. CA did not predict affective or neural responses to social rejection at age 18. Yet, CA predicted better friendships at age 14 and age 18, when adolescents with and without CA had comparable mood levels. Thus, adolescents with CA and normative mood levels have more adolescent friendship support and seem to have normal mood and neural responses to social rejection.This work was supported by grants from Friends of Peterhouse Medical Fund Cambridge (RG 51114), the Wellcome Trust (RG 074296), and the UK Medical Research Council (MC US A060 0019). JF is supported by the Medical Research Council Doctoral Training/Sackler Fund and the Pinsent Darwin Fund. JS is supported by the UK Medical Research Council (MC US A060 0019). ADA is supported by the Aker Scholarship. SS is supported by the Wellcome Trust (209127/Z/17/Z). IMG is funded by a Wellcome Trust Strategic Award and declares consulting to Lundbeck. ALvH is supported by the Royal Society (DH15017 & RGF\EA\180029 & RGF\RI\180064), and MQ (MQBFC/2). Funders of the authors played no role in the study conduction, analysis performance, or the reporting of the study

How biopsychosocial depressive risk shapes behavioral and neural responses to social evaluation in adolescence

Funder: University of Cambridge; Id: http://dx.doi.org/10.13039/501100000735Funder: MRC Cognition and Brain Sciences UnitAbstract: Introduction: Understanding the emotional responsivity style and neurocognitive profiles of depression‐related processes in at‐risk youth may be helpful in revealing those most likely to develop affective disorders. However, the multiplicity of biopsychosocial risk factors makes it difficult to disentangle unique and combined effects at a neurobiological level. Methods: In a population‐derived sample of 56 older adolescents (aged 17–20), we adopted partial least squares regression and correlation models to explore the relationships between multivariate biopsychosocial risks for later depression, emotional response style, and fMRI activity, to rejecting and inclusive social feedback. Results: Behaviorally, higher depressive risk was associated with both reduced negative affect following negative social feedback and reduced positive affect following positive social feedback. In response to both cues of rejection and inclusion, we observed a general neural pattern of increased cingulate, temporal, and striatal activity in the brain. Secondly, in response to rejection only, we observed a pattern of activity in ostensibly executive control‐ and emotion regulation‐related brain regions encompassing fronto‐parietal brain networks including the angular gyrus. Conclusion: The results suggest that risk for depression is associated with a pervasive emotional insensitivity in the face of positive and negative social feedback

Affective control in adolescence: the influence of age and depressive symptomatology on working memory

People exhibit marked individual variation in their ability to exercise cognitive control in affectively charged situations. Affective control is typically assessed in laboratory settings by comparing performance in carefully constructed executive tasks performed in both affectively neutral and affectively charged contexts. There is some evidence that affective control undergoes significant improvement throughout adolescence, though it is unclear how adolescents deemed at risk of developing depression exercise affective control despite poor affective control being identified as a contributing factor to ongoing mental ill health in adulthood. The present study therefore investigated affective control in a large (n = 425) sample of adolescents (aged 11–18 years) collected from 2016 to 2018. A simultaneous visuospatial search and written storage working memory (WM) capacity task was carried out to examine affective control, using affectively neutral and affectively negative social images as the task-irrelevant distractors. Overall, WM capacity increased as a function of age across both affective conditions. Moreover, we report a significant difference between affective conditions, with WM capacity slightly lower during trials with affectively negative social scenes, relative to neutral. Performance in each condition and the performance “cost” for completing the task in negative relative to neutral conditions was not modulated by depressive symptoms. Furthermore, age did not predict performance cost, irrespective of depressive symptoms. These findings suggest that WM capacity is relatively robust against socioaffective contexts and mood in adolescents

Franchises lost and gained: post-coloniality and the development of women’s rights in Canada

The Canadian constitution is to some extent characterised by its focus on equality, and in particular gender equality. This development of women’s rights in Canada and the greater engagement of women as political actors is often presented as a steady linear process, moving forwards from post-enlightenment modernity. This article seeks to disturb this ‘discourse of the continuous,’ by using an analysis of the pre-confederation history of suffrage in Canada to both refute a simplistic linear view of women’s rights development and to argue for recognition of the Indigenous contribution to the history of women’s rights in Canada. The gain of franchise and suffrage movements in Canada in the late nineteenth and early twentieth century are, rightly, the focus of considerable study (Pauker 2015), This article takes an alternative perspective. Instead, it examines the exercise of earlier franchises in pre-confederation Canada. In particular it analyses why franchise was exercised more widely in Lower Canada and relates this to the context of the removal of franchises from women prior to confederation

A novel Alzheimer disease locus located near the gene encoding tau protein

This is the author accepted manuscript. The final version is available from the publisher via the DOI in this recordAPOE ε4, the most significant genetic risk factor for Alzheimer disease (AD), may mask effects of other loci. We re-analyzed genome-wide association study (GWAS) data from the International Genomics of Alzheimer's Project (IGAP) Consortium in APOE ε4+ (10 352 cases and 9207 controls) and APOE ε4- (7184 cases and 26 968 controls) subgroups as well as in the total sample testing for interaction between a single-nucleotide polymorphism (SNP) and APOE ε4 status. Suggestive associations (P<1 × 10-4) in stage 1 were evaluated in an independent sample (stage 2) containing 4203 subjects (APOE ε4+: 1250 cases and 536 controls; APOE ε4-: 718 cases and 1699 controls). Among APOE ε4- subjects, novel genome-wide significant (GWS) association was observed with 17 SNPs (all between KANSL1 and LRRC37A on chromosome 17 near MAPT) in a meta-analysis of the stage 1 and stage 2 data sets (best SNP, rs2732703, P=5·8 × 10-9). Conditional analysis revealed that rs2732703 accounted for association signals in the entire 100-kilobase region that includes MAPT. Except for previously identified AD loci showing stronger association in APOE ε4+ subjects (CR1 and CLU) or APOE ε4- subjects (MS4A6A/MS4A4A/MS4A6E), no other SNPs were significantly associated with AD in a specific APOE genotype subgroup. In addition, the finding in the stage 1 sample that AD risk is significantly influenced by the interaction of APOE with rs1595014 in TMEM106B (P=1·6 × 10-7) is noteworthy, because TMEM106B variants have previously been associated with risk of frontotemporal dementia. Expression quantitative trait locus analysis revealed that rs113986870, one of the GWS SNPs near rs2732703, is significantly associated with four KANSL1 probes that target transcription of the first translated exon and an untranslated exon in hippocampus (P≤1.3 × 10-8), frontal cortex (P≤1.3 × 10-9) and temporal cortex (P≤1.2 × 10-11). Rs113986870 is also strongly associated with a MAPT probe that targets transcription of alternatively spliced exon 3 in frontal cortex (P=9.2 × 10-6) and temporal cortex (P=2.6 × 10-6). Our APOE-stratified GWAS is the first to show GWS association for AD with SNPs in the chromosome 17q21.31 region. Replication of this finding in independent samples is needed to verify that SNPs in this region have significantly stronger effects on AD risk in persons lacking APOE ε4 compared with persons carrying this allele, and if this is found to hold, further examination of this region and studies aimed at deciphering the mechanism(s) are warranted