ORCID Profile
0000-0002-9276-6358
Current Organisations
University of Sydney
,
Neuroscience Research Australia (NeuRA)
,
University of New South Wales
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Biological Psychology (Neuropsychology, Psychopharmacology, | Psychology
Publisher: Elsevier BV
Date: 2022
DOI: 10.1016/J.JPSYCHIRES.2021.11.038
Abstract: Whilst alterations in emotional face processing, as indicated by event-related potentials (ERPs), are associated with depression and anxiety symptoms in clinical and non-clinical s les, it has remained unclear whether they are related to mental wellbeing. The current study aimed to address this question in a non-clinical s le. The analysis included 402 adult twins from the TWIN-E study. The COMPAS-W and the Depression Anxiety Stress Scale (DASS-42) were used to measure mental wellbeing and depression/anxiety symptoms, respectively. Participants viewed facial expressions under Unmasked (conscious) and Masked (subliminal) conditions while ERPs were recorded. The associations of emotion processing with mental wellbeing and depression/anxiety symptoms were assessed using multivariate linear mixed models. There was a strong association between depression/anxiety symptoms and the N170 litude difference for the Fear - Happy contrast in the Masked condition after controlling for wellbeing scores (B = 0.34, p < .001). Specifically, higher depression/anxiety symptoms were associated with a lack of differentiation between fearful and happy faces. No associations were found between emotional face processing and mental wellbeing scores. These results indicate that even within a non-clinical s le, alterations in emotional ERPs, namely the N170, reflect differences in depression/anxiety symptoms rather than differences in wellbeing. Furthermore, this effect was limited to automatic processing, rather than conscious processing of emotional stimuli, suggesting the observed differences apply only to the subconscious pathway.
Publisher: CMA Joule Inc.
Date: 11-2018
DOI: 10.1503/JPN.170125
Publisher: Wiley
Date: 09-09-2020
DOI: 10.1111/GBB.12694
Publisher: Elsevier BV
Date: 09-2018
DOI: 10.1016/J.PUHE.2018.05.006
Abstract: Using data from an international collaborative research project on youth resilience in the context of migration, this study aims to investigate how different acculturation patterns (i.e. integration, assimilation, separation and marginalization) influence the mental health of migrant youth, and whether resilience might function as a mediator in the association between acculturation and mental health. A cross-sectional pilot study conducted in six countries employing a common survey questionnaire. The study s le was 194 youths aged 10-17 years (median = 13.6) from six countries (Australia, Canada, China, New Zealand, South Africa, and United Kingdom) and included cross-border and internal migrants. Mental health and well-being was measured by the Warwick-Edinburgh Mental Well-Being Scale (WEMWBS). Resilience was measured by the Child and Youth Resilience Measure-28 (CYRM-28). Acculturation was assessed using the Acculturation, Habits, and Interests Multicultural Scale for Adolescents (AHIMSA). Multivariate regression and path analysis were performed to examine the hypothesized mediation model. Resilience scores correlated strongly with mental health and well-being. Acculturation exerted no significant direct effects on the mental health of migrant youths. Nevertheless, compared to youths who were integration-oriented, assimilation-oriented youths tended to exhibit lower levels of resilience, resulting in poorer mental health. Compared to youths from other countries, migrant youths from China also reported lower levels of resilience, which led to poorer mental health outcome. Acculturation plays a significant role in the mental health of migrant youth, with different acculturative orientations exhibiting different influences through the mediation effect of resilience. Fostering resilience and facilitating integration-oriented acculturation are recommended public health strategies for migrant youth.
Publisher: Research Square Platform LLC
Date: 10-03-2022
DOI: 10.21203/RS.3.RS-1071626/V1
Abstract: The ability to perform optimally under pressure is critical across many occupations, including the military, first responders, and competitive sport, and depends on a range of cognitive factors. How common these key performance factors are across application domains remains unclear. The current study sought to integrate existing knowledge in the performance field in the form of a transdisciplinary expert consensus on the cognitive mechanisms that underlie performance under pressure. International experts were recruited from four performance domains (i. Defence ii. Competitive Sport iii. Civilian High-stakes and iv. Performance Neuroscience). Experts rated constructs from the Research Domain Criteria (RDoC) framework (in addition to several expert-suggested constructs) across successive rounds, until all constructs reached consensus for inclusion or were eliminated. Finally, included constructs were ranked for their relative importance. Sixty-eight experts completed the first Delphi round, with 94% of experts retained by the end of the Delphi process. Seven of the ten constructs that reached transdisciplinary consensus came from the Cognitive Systems domain including: 1) Attention 2) Cognitive Control—Goal Selection, Updating, Representation & Maintenance 3) Cognitive Control—Performance Monitoring 4) Cognitive Control—Response Selection & Inhibition/Suppression 5) Working memory—Flexible Updating 6) Working memory—Active Maintenance and 7) Working memory—Interference Control. Other constructs that reached transdisciplinary consensus were Self-knowledge, Arousal, and Shifting (an expert-suggested construct). Our results identify a set of transdisciplinary neuroscience-informed constructs, validated through Delphi consensus. This expert consensus is critical to standardising cognitive assessment and informing mechanism-targeted interventions in the broader field of human performance optimisation.
Publisher: Frontiers Media SA
Date: 07-09-2018
Publisher: World Scientific Pub Co Pte Lt
Date: 03-2007
DOI: 10.1142/S0219635207001398
Abstract: Following an integrative neuroscience perspective, we propose that cognitive and emotional functions are integrally linked, and that genetic polymorphisms which impact upon neural processes may have complementary effects on these functions. The brain-derived neurotrophic factor (BDNF) 66Met allele may contribute to both cognitive and emotional aspects of the depression phenotype. In 374 nonclinical subjects, BDNF genotype differences in task-related ERPs, emotion, memory, and EEG cortical arousal were examined. Using path modeling, higher negative affect in Met homozygotes was predicted by slow-wave EEG via the mediating effects of neuroticism. Both negative affect and working memory deficits were predicted by disturbances in emotion- and cognitive-related ERPs. This model held across groups with varying levels of depressed mood. Since impairments in emotion and working memory are core features of major depression, the BDNF Met allele may contribute to vulnerability for this disorder. An integrative approach in which genotypes are considered in combination with brain function and behavioral measures may be important in identifying profile markers of depression. This study directly demonstrates that cognitive and emotional neural networks are not parallel independent systems, but rather highly integrated with effects on both cognitive performance and emotional behavior.
Publisher: JMIR Publications Inc.
Date: 21-04-2022
DOI: 10.2196/34005
Abstract: Mental health has come to be understood as not merely the absence of mental illness but also the presence of mental well-being, and recent interventions have sought to increase well-being in various populations. A population that deserves particular attention is that of health care workers, whose occupations entail high levels of stress, especially given the ongoing COVID-19 pandemic. A neuroscience-based web-based well-being program for health care workers—the Thrive program—has been newly developed to promote habits and activities that contribute to brain health and overall mental well-being. This paper describes the protocol for a randomized controlled trial whose objective is to evaluate the Thrive program in comparison with an active control condition to measure whether the program is effective at increasing well-being and decreasing symptoms of psychological distress in health care workers at a designated Australian hospital. The trial will comprise two groups (intervention vs active control) and 4 measurement occasions over a 12-week period. A survey will be administered in each of weeks 0, 4, 8, and 12, and the well-being program will be delivered in weeks 1-7 (via web-based video presentations or digital p hlets). Each of the 4 surveys will comprise a range of questionnaires to measure well-being, psychological distress, and other key variables. The planned analyses will estimate group-by-time interaction effects to test the hypothesis that mental health will increase over time in the intervention condition relative to the active control condition. The Thrive program was delivered to a small number of wards at the hospital between February 2021 and July 2021, and it will be delivered to the remaining wards from October 2021 to December 2021. A power calculation has recommended a s le size of at least 200 participants in total. A linear mixed model will be used to estimate the interaction effects. This trial seeks to evaluate a new web-based well-being program for health care workers at a major public hospital. It will contribute to the growing body of research on mental well-being and ways to promote it. Australian New Zealand Clinical Trials Registry ACTRN12621000027819 8wwjut9 DERR1-10.2196/34005
Publisher: Elsevier BV
Date: 09-2014
DOI: 10.1016/J.PSYCHRES.2014.04.033
Abstract: Mental health is not simply the absence of mental illness rather it is a distinct entity representing wellness. Models of wellbeing have been proposed that emphasize components of subjective wellbeing, psychological wellbeing, or a combination of both. A new 26-item scale of wellbeing (COMPAS-W) was developed in a cohort of 1669 healthy adult twins (18-61 years). The scale was derived using factor analysis of multiple scales of complementary constructs and confirmed using tests of reliability and convergent validity. Bivariate genetic modeling confirmed its heritability. From an original 89 items we identified six independent subcomponents that contributed to wellbeing. The COMPAS-W scale and its subcomponents showed construct validity against psychological and physical health behaviors, high internal consistency (average r=0.71, Wellbeing r=0.84), and 12-month test-retest reliability (average r=0.62, Wellbeing r=0.82). There was a moderate contribution of genetics to total Wellbeing (heritability h(2)=48%) and its subcomponents: Composure (h(2)=24%), Own-worth (h(2)=42%), Mastery (h(2)=40%), Positivity (h(2)=42%), Achievement (h(2)=32%) and Satisfaction (h(2)=43%). Multivariate genetic modeling indicated genetic variance was correlated across the scales, suggesting common genetic factors contributed to Wellbeing and its subcomponents. The COMPAS-W scale provides a validated indicator of wellbeing and offers a new tool to quantify mental health.
Publisher: Springer Science and Business Media LLC
Date: 20-01-2009
DOI: 10.1038/MP.2008.143
Abstract: In idual risk markers for depression and anxiety disorders have been identified but the explicit pathways that link genes and environment to these markers remain unknown. Here we examined the explicit interactions between the brain-derived neurotrophic factor (BDNF) Val66Met gene and early life stress (ELS) exposure in brain (amygdala-hippoc al-prefrontal gray matter volume), body (heart rate), temperament and cognition in 374 healthy European volunteers assessed for depression and anxiety symptoms. Brain imaging data were based on a subset of 89 participants. Multiple regression analysis revealed main effects of ELS for body arousal (resting heart rate, P=0.005) and symptoms (depression and anxiety, P<0.001) in the absence of main effects for BDNF. In addition, significant BDNF-ELS interactions indicated that BDNF Met carriers exposed to greater ELS have smaller hippoc al and amygdala volumes (P=0.013), heart rate elevations (P=0.0002) and a decline in working memory (P=0.022). Structural equation path modeling was used to determine if this interaction predicts anxiety and depression by mediating effects on the brain, body and cognitive measures. The combination of Met carrier status and exposure to ELS predicted reduced gray matter in hippoc us (P<0.001), and associated lateral prefrontal cortex (P<0.001) and, in turn, higher depression (P=0.005). Higher depression was associated with poorer working memory (P=0.005), and slowed response speed. The BDNF Met-ELS interaction also predicted elevated neuroticism and higher depression and anxiety by elevations in body arousal (P<0.001). In contrast, the combination of BDNF V/V genotype and ELS predicted increases in gray matter of the amygdala (P=0.003) and associated medial prefrontal cortex (P<0.001), which in turn predicted startle-elicited heart rate variability (P=0.026) and higher anxiety (P=0.026). Higher anxiety was linked to verbal memory, and to impulsivity. These effects were specific to the BDNF gene and were not evident for the related 5HTT-LPR polymorphism. Overall, these findings are consistent with the correlation of depression and anxiety, yet suggest that partially differentiated gene-brain cognition pathways to these syndromes can be identified, even in a nonclinical s le. Such findings may aid establishing an evidence base for more tailored intervention strategies.
Publisher: Elsevier BV
Date: 07-2010
DOI: 10.1016/J.NEULET.2010.04.071
Abstract: Recent studies suggest that resting posterior versus frontal EEG delta/theta activity (delta/theta Pz-Fz) is both sensitive to pharmacological manipulations of neural dopamine and associated with the agency facet of extraversion (i.e., a motivational disposition comprising enthusiasm, energy, assertiveness, achievement striving and social dominance). These observations suggest that posterior versus frontal resting EEG delta/theta activity may represent a useful marker for investigating the molecular genetic basis of extraversion. The present study aimed to test the novel hypothesis of an association between delta/theta Pz-Fz and a functional polymorphism of the enzyme catechol-O-methyltransferase (COMT VAL(158)MET) involved in dopamine catabolism. This was conducted in a large EEG data set from the Brain Resource International Database (BRID resting EEG from N=1093 healthy in iduals, 382 of which also genotyped for COMT VAL(158)MET). In summary, we (1) showed for the first time that the VAL allele is associated with increased delta/theta Pz-Fz (2) replicated the association between extraversion and delta/theta Pz-Fz in a large, heterogeneous s le including both genders and (3) documented that the VAL allele of the COMT VAL(158)MET is associated with increased extraversion scores, as previously reported for an overlapping BRID s le. This coherent pattern of findings adds further support to the suggestion that the posterior-anterior distribution of resting EEG slow wave activity in the delta/theta range represents a useful tool for probing the dopaminergic basis of extraversion.
Publisher: American Psychological Association (APA)
Date: 08-2017
DOI: 10.1037/EMO0000300
Abstract: Previous studies have established that personality traits related to emotionality are moderately heritable. However, the relative heritability of the strategies people use to regulate emotions is unknown. The present study compared the magnitude of additive genetic, shared environmental, and nonshared environmental influences on 2 commonly used emotion regulation strategies: cognitive reappraisal and expressive suppression. In 743 twin pairs (1,486 twins), we replicated previous estimates of heritability of neuroticism (a2 = .41). Furthermore, cognitive reappraisal was significantly less heritable and more influenced by nonshared environment (a2 = .20 e2 = .80) than either neuroticism or suppression (a2 = .35 e2 = .65), another emotion regulation strategy. Finally, Cholesky decomposition modeling suggested that while there were common genetic and environmental influences on neuroticism, reappraisal and suppression, there were also significant nonshared environmental influences common between reappraisal and adaptive emotional functioning after controlling for neuroticism and suppression. These findings highlight that different aspects of emotional processing, even the use of different emotion regulation strategies, are differentially heritable. The importance of the nonshared environmental influences specific to reappraisal and adaptive emotional functioning speaks to the potential impact of social context, social partners, and psychosocial interventions on reappraisal habits. (PsycINFO Database Record
Publisher: SAGE Publications
Date: 09-03-2019
Abstract: Posttraumatic stress disorder and childhood trauma frequently co-occur. Both are associated with abnormal neural responses to salient emotion stimuli. As childhood trauma is a risk factor for posttraumatic stress disorder, differentiating between their neurophysiological effects is necessary to elucidate the neural pathways by which childhood trauma exposure contributes to increased posttraumatic stress disorder risks. Face-specific N170 evoked response potentials for backward-masked (non-conscious) and conscious threat (fear, angry) and non-threat (happy) faces were measured in 77 adults (18–64 years old, 64% women, 78% right-handed) symptomatic for posttraumatic stress disorder. Differences in N170 peak litudes for fear-versus-happy and angry-versus-happy faces at bilateral temporo-occipital (T5, T6) sites were computed. The effect of cumulative exposure to childhood interpersonal trauma, other childhood trauma, adult trauma, depression and posttraumatic stress disorder symptom severity on the N170 response was assessed using hierarchical multiple regression analyses. T5 N170 peak litudes for non-conscious fear-versus-happy faces were inversely related to cumulative childhood interpersonal trauma after accounting for socio-demographic, clinical symptom and other trauma factors. Posttraumatic stress disorder Avoidance was positively associated with N170 peak litudes for non-conscious fear-versus-happy faces, primarily due to reduced N170 responsivity to happy faces. Childhood interpersonal trauma exposure is associated with reduced discrimination between fear and happy faces, while avoidance symptom severity is associated with d ened responsivity to automatically processed happy faces in posttraumatic stress disorder adults. Results are discussed in terms of the likely contributions of impaired threat discrimination and deficient reward processing during neural processing of salient emotion stimuli, to increased risks of posttraumatic stress disorder onset and chronicity in childhood interpersonal trauma–exposed adults.
Publisher: Elsevier BV
Date: 08-2007
DOI: 10.1016/J.NEUROIMAGE.2007.05.011
Abstract: Loss-of-function mutations in MCPH1 and ASPM are responsible for some cases of autosomal recessive primary microcephaly. Recent studies have indicated that certain common variants of these genes have been positively selected for during the evolution of modern humans. It is therefore possible that these variants may predispose to an increase in brain size in the normal human population. We genotyped the MCPH1 G37995C and ASPM A44871G polymorphisms in a cohort of 118 healthy people who had undergone structural magnetic resonance imaging analysis. We did not detect significant association of either MCPH1 G37995C or ASPM A44871G genotype with whole brain volume, cerebral cortical volume or proportion of grey matter in this cohort. Nor did we detect an association of combined MCPH1 37995C and ASPM 44871G allele dosage with these brain measurements. These results were also confirmed in an age-restricted subcohort of 94 in iduals. This study suggests that phenotypes other than brain size may have been selected for in ASPM and MCPH1 variants during evolution of modern humans.
Publisher: Cambridge University Press (CUP)
Date: 11-01-2023
DOI: 10.1017/S0033291721005262
Abstract: While previous studies have suggested that higher levels of cognitive performance may be related to greater wellbeing and resilience, little is known about the associations between neural circuits engaged by cognitive tasks and wellbeing and resilience, and whether genetics or environment contribute to these associations. The current study consisted of 253 monozygotic and dizygotic adult twins, including a subs le of 187 early-life trauma-exposed twins, with functional Magnetic Resonance Imaging data from the TWIN-E study. Wellbeing was measured using the COMPAS-W Wellbeing Scale while resilience was defined as a higher level of positive adaptation (higher levels of wellbeing) in the presence of trauma exposure. We probed both sustained attention and working memory processes using a Continuous Performance Task in the scanner. We found significant negative associations between resilience and activation in the bilateral anterior insula engaged during sustained attention. Multivariate twin modelling showed that the association between resilience and the left and right insula activation was mostly driven by common genetic factors, accounting for 71% and 87% of the total phenotypic correlation between these variables, respectively. There were no significant associations between wellbeing/resilience and neural activity engaged during working memory updating. The findings suggest that greater resilience to trauma is associated with less activation of the anterior insula during a condition requiring sustained attention but not working memory updating. This possibly suggests a pattern of ‘neural efficiency’ (i.e. more efficient and/or attenuated activity) in people who may be more resilient to trauma.
Publisher: Elsevier BV
Date: 10-2016
DOI: 10.1016/J.PSYCHRES.2016.07.016
Abstract: Mental wellbeing and mental illness symptoms are typically conceptualized as opposite ends of a continuum, despite only sharing about a quarter in common variance. We investigated the normative variation in measures of wellbeing and of depression and anxiety in 1486 twins who did not meet clinical criteria for an overt diagnosis. We quantified the shared versus distinct genetic and environmental variance between wellbeing and depression and anxiety symptoms. The majority of participants (93%) reported levels of depression and anxiety symptoms within the healthy range, yet only 23% reported a wellbeing score within the "flourishing" range: the remainder were within the ranges of "moderate" (67%) or "languishing" (10%). In twin models, measures of wellbeing and of depression and anxiety shared 50.09% of variance due to genetic factors and 18.27% due to environmental factors the rest of the variance was due to unique variation impacting wellbeing or depression and anxiety symptoms. These findings suggest that an absence of clinically-significant symptoms of depression and anxiety does not necessarily indicate that an in idual is flourishing. Both unique and shared genetic and environmental factors may determine why some in iduals flourish in the absence of symptoms while others do not.
Publisher: Elsevier BV
Date: 05-2015
DOI: 10.1016/J.JAD.2015.01.061
Abstract: Depressed patients with melancholic features have distinct impairments in cognition and anhedonia, but it remains unknown whether these impairments can be quantified on neurocognitive biomarker tests of behavioral performance. We compared melancholic major depressive disorder (MDD) patients to non-melancholic MDD patients and controls on a neurocognitive test battery that assesses eight general and emotional cognitive domains including the hypothesized decision-making and reward-threat perception. MDD outpatients (n=1008) were assessed using a computerized battery of tests. MDD participants met DSM-IV criteria for MDD and had a score ≥16 on the 17-item Hamilton Rating Scale for Depression. Melancholic MDD was defined using the Mini-International Neuropsychiatric Interview and a psychomotor disturbance observer-rated CORE measure score >7. Controls were age- and gender-matched with no previous DSM-IV or significant medical history. Melancholic participants (33.7% of the MDD s le) exhibited significantly poorer performance than controls across each domain of cognitive function and for speed of emotion identification and implicit emotion priming. Compared to the non-melancholic group, specific disturbances were seen on tests of information speed, decision speed, and reward-relevant emotional processing of happy expressions, even after co-varying for symptom severity. Assessments were taken at only one medication-free time point. Reward was investigated using an emotional faces task. Melancholic MDD is distinguished by a specific neurocognitive marker profile consistent with reduced decision-making capacity under time demands and loss of reward sensitivity. This profile suggests an underlying deficit in mesolimbic-cortical circuitry for motivationally-directed behavior.
Publisher: Elsevier BV
Date: 2013
DOI: 10.1016/J.JPSYCHIRES.2012.08.006
Abstract: Exposure to early life trauma is a known risk factor for depression and anxiety disorders in adulthood. This study aimed to evaluate the relative contributions of early life versus adult trauma in predicting levels of depressive and anxiety symptoms in nonclinical community adults. 1209 nonclinical community adults (18-70 years 45% male) were assessed for mental health status, early life stressors, lifetime trauma exposure, and self-reported levels of depressive and anxiety symptoms. A subset of the full s le subjected to group comparisons (n = 1088) indicated that early life stressor exposure primarily accounted for significantly higher depressive and anxiety symptom scores when compared against adults reporting to be free of childhood stressor or adult trauma exposure. Subsequent hierarchical multiple regression analyses of this subset using five distinct early life stressor types, namely 'Interpersonal violation', 'Family breakup', 'Disasters/war', 'Familial health trauma/death' and 'Personal health trauma' derived from principal component analysis of a wide range of self-reported early stressor events in the full s le, showed childhood 'Interpersonal violation' differentially predicted higher self-reported depressive and anxiety symptom scores in both males and females. Adult trauma exposure did not significantly predict these symptom scores. These findings underline the relative importance of exposure to 'interpersonal violation' relative to other types of early life stressors and adult trauma in the risk of depressive and anxiety symptoms in nonclinical community adults.
Publisher: Elsevier BV
Date: 06-2010
DOI: 10.1016/J.BIOPSYCH.2009.12.012
Abstract: Depression is associated with an increase in the likelihood of cardiac events however, studies investigating the relationship between depression and heart rate variability (HRV) have generally focused on patients with cardiovascular disease (CVD). The objective of the current report is to examine with meta-analysis the impact of depression and antidepressant treatment on HRV in depressed patients without CVD. Studies comparing 1) HRV in patients with major depressive disorder and healthy control subjects and 2) the HRV of patients with major depressive disorder before and after treatment were considered for meta-analysis. Meta-analyses were based on 18 articles that met inclusion criteria, comprising a total of 673 depressed participants and 407 healthy comparison participants. Participants with depression had lower HRV (time frequency: Hedges' g = -.301, p < .001 high frequency: Hedges' g = -.293, p < .001 nonlinear: Hedges' g = -1.955, p = .05 Valsalva ratio: Hedges' g = -.712, p < .001) than healthy control subjects, and depression severity was negatively correlated with HRV (r = -.354, p < .001). Tricyclic medication decreased HRV, although serotonin reuptake inhibitors, mirtazapine, and nefazodone had no significant impact on HRV despite patient response to treatment. Depression without CVD is associated with reduced HRV, which decreases with increasing depression severity, most apparent with nonlinear measures of HRV. Critically, a variety of antidepressant treatments do not resolve these decreases despite resolution of symptoms, highlighting that antidepressant medications might not have HRV-mediated cardioprotective effects and the need to identify in iduals at risk among patients in remission.
Publisher: Springer Science and Business Media LLC
Date: 08-10-2022
DOI: 10.1007/S00586-022-07404-7
Abstract: To evaluate the relationship between lifestyle behaviours, emotional health factors, and low back pain (LBP) resilience. This retrospective longitudinal study utilised 1,065 twins with a recent history of LBP from the Washington State Twin Registry. A lifestyle behaviour score was built using variables of body mass index, physical activity engagement, sleep quality, smoking status, and alcohol consumption. An emotional health score was built using variables of the absence of depressed mood, perceived stress, and active coping. The main outcome was LBP resilience, assessed as recovery (“bouncing back”), and sustainability (maintaining high levels of function despite LBP). After adjusting for covariates, there was no relationship between the lifestyle behaviour score (OR 1.05, 95% CI 0.97–1.15, p = 0.218) and the emotional health score (OR 1.08, 95% CI 0.98–1.19, p = 0.142) with the likelihood of recovering from LBP. There was however, evidence of a positive association between the lifestyle behaviour score ( β 0.20, 95% CI 0.04–0.36, p = 0.013), the emotional health score ( β 0.22, 95% CI 0.00–0.43, p = 0.049), and greater levels of sustainability. These results were confirmed by a within-pair analysis (lifestyle behaviour score: β 1.79, 95% CI 0.05–3.53, p = 0.043) and (emotional health score: β 0.52, 95% CI 0.09–0.96, p = 0.021) adjusting for genetic and early shared environmental confounding. Findings from this study suggest that people who adopt optimal lifestyle behaviours and positive emotional factors are more likely to be resilient and maintain high levels of function despite suffering from LBP.
Publisher: Elsevier BV
Date: 02-2021
Publisher: Springer Science and Business Media LLC
Date: 17-10-2017
DOI: 10.1038/TP.2017.204
Abstract: Although advances in neuroimaging have yielded insights into the intrinsic organization of human brain networks and their relevance to psychiatric and neurological disorders, there has been no translation of these insights into clinical practice. One necessary step toward clinical translation is identifying a summary metric of network function that is reproducible, reliable, and has known normative data, analogous to normed neuropsychological tests. Our aim was therefore to establish the proof of principle for such a metric, focusing on the default mode network (DMN). We compared three candidate summary metrics: global clustering coefficient, characteristic path length, and average connectivity. Across three s les totaling 322 healthy, mostly Caucasian adults, average connectivity performed best, with good internal consistency (Cronbach’s α =0.69–0.70) and adequate eight-week test–retest reliability (intra-class coefficient=0.62 in a subs le N =65). We therefore present normative data for average connectivity of the DMN and its sub-networks. These proof of principle results are an important first step for the translation of neuroimaging to clinical practice. Ultimately, a normed summary metric will allow a single patient’s DMN function to be quantified and interpreted relative to normative peers.
Publisher: Elsevier BV
Date: 07-2007
DOI: 10.1016/J.BIOPSYCHO.2007.03.001
Abstract: Neuroimaging shows brain-functional differences due to apolipoprotein E (APOE) polymorphisms may exist decades before the increased risk period for Alzheimer's disease, but little is known about their effect on cognition and brain function in children and young adults. This study assessed 415 healthy epsilon2 and epsilon4 carriers and matched epsilon3/epsilon3 controls, spanning ages 6-65, on a range of cognitive tests. Subjects were also compared on a new dynamical measure of EEG activity during a visual working memory task using alphabetical stimuli. epsilon4 subjects had better verbal fluency compared to epsilon3, an effect that was strongest in 51-65 year-olds. No epsilon4 deficits in cognition were found. In 6-15 year-olds, there were differences in total spatio-temporal wave activity between epsilon3 and epsilon4 subjects in the theta band, approximately 200ms post-stimulus. Differences in brain function in younger epsilon4 subjects and superior verbal fluency across the entire age range suggest that the APOE epsilon4 allele is an ex le of antagonistic pleiotropy.
Publisher: Wiley
Date: 04-09-2019
DOI: 10.1002/EJP.1304
Abstract: Alterations in the grey matter volume of several brain regions have been reported in people with chronic pain. The most consistent observation is a decrease in grey matter volume in the medial prefrontal cortex. These findings are important as the medial prefrontal cortex plays a critical role in emotional and cognitive processing in chronic pain. Although a logical cause of grey matter volume decrease may be neurodegeneration, this is not supported by the current evidence. Therefore, the purpose of this review was to evaluate the existing literature to unravel what the decrease in medial prefrontal cortex grey matter volume in people with chronic pain may represent on a biochemical and cellular level. A literature search for this topical review was conducted using PubMed and SCOPUS library. Search terms included chronic pain, pain, medial prefrontal cortex, anterior cingulate cortex, grey matter, neurochemistry, spectroscopy, magnetic resonance imaging, positron emission tomography, dendrite, neurodegeneration, glia, astrocyte, microglia, neurotransmitter, glutamate, GABA and different combinations of these terms. Adopting a stress model of chronic pain, two major pathways are proposed that contribute to grey matter volume decrease in the medial prefrontal cortex: (a) changes in dendritic morphology as a result of hypothalamic-pituitary axis dysfunction and (b) neurotransmitter dysregulation, specifically glutamate and γ-Aminobutyric acid, which affects local microvasculature. Our model proposes new mechanisms in chronic pain pathophysiology responsible for mPFC grey matter loss as alternatives to neurodegeneration. It is unclear what the decrease in medial prefrontal cortex grey matter volume represents in chronic pain. The most attractive reason is neurodegeneration. However, there is no evidence to support this. Our review reveals nondegenerative causes of decreased medial prefrontal grey matter to guide future research into chronic pain pathophysiology.
Publisher: Elsevier BV
Date: 09-2009
DOI: 10.1016/J.NEUROIMAGE.2009.05.009
Abstract: The INTEGRATE Model draws on the framework of 'integrative neuroscience' to bring together brain-body and behavioral concepts of emotion, thinking and feeling and their regulation. The key organizing principle is the drive to 'minimize danger and maximize reward' that determines what is significant to us at each point in time. Traits of 'negativity bias' reflect the tendency to perceive danger rather than reward related information, and this bias influences emotion, thinking and feeling processes. Here, we examined a self-report measure of Negativity Bias in relation to its impact on brain and body correlates of emotion processing. The contributions of the serotonin transporter (5-HTT-LPR) allelic variants and early life stress to both negativity bias and these correlates were also examined. Data were accessed in collaboration with the Brain Resource International Database (BRID) which provides standardized data across these domains of measurement. From an initial s le of 303 nonclinical subjects from the BRID, subjects scoring one standard deviation below (n=55) and above (n=47) the mean on the measure of negativity bias were identified as 'Negativity Bias' and 'Positivity Bias' groups for analysis, respectively. These subjects had been genotyped for 5-HTT-LPR Short allele versus LL homozygote status, and completed the early life stress scale, and recording of startle responses and heart rate for conscious and nonconscious fear conditions. A matched subset (n=39) of BRID subjects completed functional MRI with the same facial emotion tasks. The Negativity Bias (compared to Positivity Bias) group was distinguished by both arousal and brain function correlates: higher startle litude, higher heart rate for conscious and nonconscious fear conditions, and heightened activation in neural circuitry for both fear conditions. Regions of heightened activation included brainstem and bilateral amygdala, anterior cingulate and ventral and dorsal medial prefrontal cortex (mPFC) for conscious fear, and brainstem and right-sided amygdala, anterior cingulate and ventral, mPFC for nonconscious fear. The 5-HTT-LPR Short allele (versus LL) conferred a similar pattern of arousal and neural activation. For those with the 5-HTT-LPR Short allele, the addition of early life stress contributed to enhanced negativity bias, and to further effects on heart rate and neural activation for nonconscious fear in particular. These findings suggest that traits of negativity bias impact brain-body arousal correlates of fear circuitry. Both genetic variation and life stressors contribute to the impact of negativity bias. Given that negativity bias is a feature of conditions such as depression and associated biological alterations, the findings have implications for translation into clinical decision support.
Publisher: Public Library of Science (PLoS)
Date: 20-09-2013
Publisher: Elsevier BV
Date: 11-2017
Publisher: Elsevier BV
Date: 2016
DOI: 10.1016/J.CLINPH.2015.05.032
Abstract: To determine whether EEG occipital alpha and frontal alpha asymmetry (FAA) distinguishes outpatients with major depression (MDD) from controls, predicts antidepressant treatment outcome, and to explore the role of gender. In the international Study to Predict Optimized Treatment in Depression (iSPOT-D), a multi-center, randomized, prospective open-label trial, 1008 MDD participants were randomized to escitalopram, sertraline or venlafaxine-extended release. The study also recruited 336 healthy controls. Treatment response was established after eight weeks and resting EEG was measured at baseline (two minutes eyes open and eyes closed). No differences in EEG alpha for occipital and frontal cortex, or for FAA, were found in MDD participants compared to controls. Alpha in the occipital and frontal cortex was not associated with treatment outcome. However, a gender and drug-class interaction effect was found for FAA. Relatively greater right frontal alpha (less cortical activity) in women only was associated with a favorable response to the Selective Serotonin Reuptake Inhibitors escitalopram and sertraline. No such effect was found for venlafaxine-extended release. FAA does not differentiate between MDD and controls, but is associated with antidepressant treatment response and remission in a gender and drug-class specific manner. Future studies investigating EEG alpha measures in depression should a-priori stratify by gender.
Publisher: Informa UK Limited
Date: 30-09-2016
DOI: 10.1080/02699931.2016.1232242
Abstract: Alterations to cognitive function are often reported with depression and anxiety symptoms, yet few studies have examined the same associations with mental well-being. This study examined the association between mental well-being, depression and anxiety symptoms and cognitive function in 1502 healthy adult monozygotic (MZ) and dizygotic (DZ) twins, and the shared/unique contribution of genetic (G) and environmental (E) variance. Using linear mixed models, mental well-being was positively associated (p < .01) with sustained attention (β = 0.127), inhibition (β = 0.096), cognitive flexibility (β = 0.149), motor coordination (β = 0.114) and working memory (β = 0.156), whereas depression and anxiety symptoms were associated (p < .01) with poorer sustained attention (β = -0.134), inhibition (β = -0.139), cognitive flexibility (β = -0.116) and executive function (β = -0.139). Bivariate twin modelling showed well-being shared a small environmental correlation with motor coordination and a small genetic correlation with working memory. Trivariate twin modelling showed well-being shared a small genetic correlation with inhibition, whereas depression and anxiety symptoms shared a small environmental correlation with inhibition. The remaining variance was mostly driven by unique G and/or E variance. Overall, well-being and depression and anxiety symptoms show both independent and shared relationships with cognitive functions but this is largely attributable to unique G or E variance and small shared G/E variance between pairs of variables.
Publisher: Elsevier BV
Date: 10-2008
DOI: 10.1016/J.BIOPSYCHO.2008.07.004
Abstract: A functional polymorphism of the brain-derived neurotrophic factor, BDNF Val66Met, is associated with risk for major depression alongside impairments in memory and selective attention. This study aims to identify the mediating neural mechanisms in links between BDNF and depression using highly heritable electroencephalographic (EEG) recordings. In 305 healthy subjects, BDNF Val66Met genotypes were compared in terms of trait depression, neural function (EEG during a resting state) and cognitive performance. The mediating effects of the EEG brain imaging endophenotypes were also examined using structural equation (path) modeling. A genotype-endophenotype-phenotype path model showed that Met homozygosity predicted elevated working memory commission errors and altered EEG activity that is elevated relative theta and delta power coupled with reduced alpha power. In turn, reduced EEG alpha activity mediated the relationship between the Met/Met genotype and trait depression. These findings demonstrate the utility of an integrative endophenotype approach. They suggest that the BDNF Met/Met homozygote has a direct impact on memory systems, but impacts trait depression via the secondary effects of neural changes.
Publisher: Frontiers Media SA
Date: 05-2018
Publisher: Cambridge University Press (CUP)
Date: 06-2012
DOI: 10.1017/THG.2012.12
Abstract: Despite the significant advancements being made in the neurogenetics for mental health, the identification and validation of potential endophenotype markers of risk and resilience remain to be confirmed. The TWIN-E study (The Twin study in Wellbeing using Integrative Neuroscience of Emotion) aims to validate endophenotype markers of mental health across cognitive, brain, and autonomic measures by testing the heritability, clinical plausibility, and reliability of each of these measures in a large adult twin cohort. The specific gene and environmental mechanisms that moderate prospective links between endophenotype-phenotype markers and the final outcome of wellbeing will also be identified. TWIN-E is a national prospective study with three phases: I) baseline testing on a battery of online questionnaires and cognitive tasks, and EEG, MRI, and autonomic testing II) 12-month follow-up testing on the online assessments and III) randomized controlled trial of brain training. Minimum target numbers include 1,500 male/female twins (18–65 years) for the online assessments (Phase I and II), 300 twins for the EEG testing component, and 244 twins for the MRI testing component. For Phase III, each twin out of the pair will be randomized to either the treatment or waitlist control group to test the effects of brain training on mental health over a 30-day period, and to confirm the gene–environment and endophenotype contributions to treatment response. Preliminary heritability results are provided for the first 50% of the MRI subgroup ( n = 142) for the grey matter volume, thickness, and surface area measures, and white matter diffuse tensor imaging fractional anisotropy.
Publisher: Springer Science and Business Media LLC
Date: 19-03-2022
DOI: 10.1038/S41398-022-01874-5
Abstract: Wellbeing is an important aspect of mental health that is moderately heritable. Specific wellbeing-related variants have been identified via GWAS meta-analysis of in idual questionnaire items. However, a multi-item within-subject index score has potential to capture greater heritability, enabling improved delineation of genetic and phenotypic relationships across traits and exposures that are not possible on aggregate-data. This research employed data from the UK Biobank resource, and a wellbeing index score was derived from indices of happiness and satisfaction with family/friendship/finances/health, using principal component analysis. GWAS was performed in Caucasian participants ( N = 129,237) using the derived wellbeing index, followed by polygenic profiling (independent s le N = 23,703). The wellbeing index, its subcomponents, and negative indicators of mental health were compared via phenotypic and genetic correlations, and relationships with psychiatric disorders examined. Lastly, the impact of childhood maltreatment on wellbeing was investigated. Five independent genome-wide significant loci for wellbeing were identified. The wellbeing index had SNP-heritability of ~8.6%, and stronger phenotypic and genetic correlations with its subcomponents (0.55–0.77) than mental health phenotypes (−0.21 to −0.39). The wellbeing score was lower in participants reporting various psychiatric disorders compared to the total s le. Childhood maltreatment exposure was also associated with reduced wellbeing, and a moderate genetic correlation ( r g = ~−0.56) suggests an overlap in heritability of maltreatment with wellbeing. Thus, wellbeing is negatively associated with both psychiatric disorders and childhood maltreatment. Although notable limitations, biases and assumptions are discussed, this within-cohort study aids the delineation of relationships between a quantitative wellbeing index and indices of mental health and early maltreatment.
Publisher: Elsevier BV
Date: 12-2014
Publisher: Wiley
Date: 11-06-2009
DOI: 10.1002/HBM.20592
Publisher: Elsevier BV
Date: 11-2010
DOI: 10.1016/J.BIOPSYCH.2010.06.025
Abstract: Depression will be the second largest burden of disease by 2020. Developing new tools for identifying risk and ultimately prevention of depression relies on elucidating the integrative relationships between susceptibility markers from gene-stress interactions and how they impact emotional brain and arousal systems. They have largely been studied in isolation. We examined how genetic (brain-derived neurotrophic factor [BDNF] valine 66 to methionine [Val66Met] and serotonin receptor gene 3A [HTR3A]) and early life stress susceptibility factors interact in predicting electroencephalogram (EEG) asymmetry, emotion-elicited heart rate, and self-reported negativity bias, each correlates of risk for depression. Caucasian volunteers (n = 363) were derived from the Brain Resource International Database, via the Brain Research And Integrative Neuroscience Network. In iduals with both BDNF methionine and HTR3A CC risk genotypes and early life stressors demonstrated a profile of elevated emotion-elicited heart rate and right frontal hyper-activation with right parietotemporal hypoactivation in EEG asymmetry. Elevations in heart rate were a moderator of negativity bias. The findings provide new evidence that these gene-stress susceptibility factors contribute to a brain-arousal profile indicative of risk for depression. They are a step toward identifying biological markers for detecting risk before overt symptoms. It would be valuable for future studies to examine comorbidity and specificity issues for instance, whether these gene-stress factors contribute in different ways to the partially distinct EEG asymmetry profiles found with anxiety.
Publisher: World Scientific Pub Co Pte Lt
Date: 09-2008
DOI: 10.1142/S0219635208001939
Abstract: This study was undertaken using the INTEGRATE Model of brain organization, which is based on a temporal continuum of emotion, thinking and self regulation. In this model, the key organizing principle of self adaption is the motivation to minimize danger and maximize reward. This principle drives brain organization across a temporal continuum spanning milliseconds to seconds, minutes and hours. The INTEGRATE Model comprises three distinct processes across this continuum. Emotion is defined by automatic action tendencies triggered by signals that are significant due to their relevance to minimizing danger-maximizing reward (such as abrupt, high contrast stimuli). Thinking represents cognitive functions and feelings that rely on brain and body feedback emerging from around 200 ms post-stimulus onwards. Self regulation is the modulation of emotion, thinking and feeling over time, according to more abstract adaptions to minimize danger-maximize reward. Here, we examined the impact of dispositional factors, age and genetic variation, on this temporal continuum. Brain Resource methodology provided a standardized platform for acquiring genetic, brain and behavioral data in the same 1000 healthy subjects. Results showed a "paradox" of declining function in the "thinking" time scale over the lifespan (6 to 80+ years), but a corresponding preservation or even increase in automatic functions of "emotion" and "self regulation". This paradox was paralleled by a greater loss of grey matter in cortical association areas (assessed using MRI) over age, but a relative preservation of subcortical grey matter. Genetic polymorphisms associated with both healthy function and susceptibility to disorder (including the BDNFVal(66)Met, COMTVal(158/108)Met, MAOA and DRD4 tandem repeat and 5HTT-LPR polymorphisms) made specific contributions to emotion, thinking and self regulatory functions, which also varied according to age.
Publisher: Springer Science and Business Media LLC
Date: 04-02-2009
DOI: 10.1038/NPP.2009.1
Abstract: Association studies suggest that the low activity variant of the monoamine oxidase A (MAOA)-uVNTR polymorphism confers risk for emotional disturbances associated with antisocial traits, particularly in males. Here, we assessed the low (MAOA-L) activity variant in relation to both brain function and a behavioral index of antisocial traits. From an initial s le of 290 healthy participants, 210 had low (MAOA-L) or high (MAOA-H) activity variants. Participants underwent a brief assessment of personality traits and event-related potential (ERP) recording during an emotion-processing task. Genotype differences in ERPs were localized using LORETA. The MAOA-L genotype was distinguished by elevated scores on the index of antisocial traits. These traits were related to altered ERPs elicited 120-280ms post-stimulus, particularly for negative emotion. Altered neural processing of anger in MAOA-L genotypes was localized to medial frontal, parietal, and superior temporo-occipital regions in males, but only to the superior occipital cortex in females. The MAOA low activity variant may increase susceptibility to antisocial traits through alterations to the neural systems for processing threat-related emotion, especially for males. Monoamines such as noradrenalin and serotonin may modulate these relationships, given that their metabolism varies according to MAOA variants, and that they modulate both emotional brain systems and antisocial aggression.
Publisher: Hindawi Limited
Date: 08-2010
DOI: 10.1002/DA.20726
Abstract: The risk for mental illnesses such as depression is increasingly conceptualized as the product of gene-environment interactions and their impact on brain structure and function. The role of serotonin 3A receptor gene (HTR3A -42C>T polymorphism) and its interaction with early life stress (ELS) was investigated in view of the receptor's localization to brain regions central to emotion processing. Fronto-limbic grey matter (GM) loss was measured using magnetic resonance imaging and assessed using voxel-based morphometry analysis in 397 nonclinical in iduals from the Brain Resource International Database. Negative mood symptoms were also assessed. The HTR3A CC genotype group, compared to the T carriers, demonstrated comparative loss to GM in hippoc al structures, which extended to the frontal cortices for those CC genotype in iduals also exposed to ELS. Elevations in depressed mood were also evident. These findings suggest that the HTR3A CC genotype may be associated with alterations in brain structures central to emotion processing, particularly when exposed to stress, and further highlight the potential role of the serotonin system in the pathophysiology of affective disorders. In contrast, those in iduals with the T allele, in particular the TT genotype, may be more protected from such alterations combined with minimal exposure to ELS events.
Publisher: Elsevier BV
Date: 06-2018
DOI: 10.1016/J.PSYCHRES.2018.03.042
Abstract: Currently there is a very limited understanding of how mental wellbeing versus anxiety and depression symptoms are associated with emotion processing behaviour. For the first time, we examined these associations using a behavioural emotion task of positive and negative facial expressions in 1668 healthy adult twins. Linear mixed model results suggested faster reaction times to happy facial expressions was associated with higher wellbeing scores, and slower reaction times with higher depression and anxiety scores. Multivariate twin modelling identified a significant genetic correlation between depression and anxiety symptoms and reaction time to happy facial expressions, in the absence of any significant correlations with wellbeing. We also found a significant negative phenotypic relationship between depression and anxiety symptoms and accuracy for identifying neutral emotions, although the genetic or environment correlations were not significant in the multivariate model. Overall, the phenotypic relationships between speed of identifying happy facial expressions and wellbeing on the one hand, versus depression and anxiety symptoms on the other, were in opposing directions. Twin modelling revealed a small common genetic correlation between response to happy faces and depression and anxiety symptoms alone, suggesting that wellbeing and depression and anxiety symptoms show largely independent relationships with emotion processing at the behavioral level.
Publisher: Springer Science and Business Media LLC
Date: 05-09-2021
Publisher: JMIR Publications Inc.
Date: 03-10-2021
Abstract: ental health has come to be understood as not merely the absence of mental illness but also the presence of mental well-being, and recent interventions have sought to increase well-being in various populations. A population that deserves particular attention is that of health care workers, whose occupations entail high levels of stress, especially given the ongoing COVID-19 pandemic. A neuroscience-based web-based well-being program for health care workers—the Thrive program—has been newly developed to promote habits and activities that contribute to brain health and overall mental well-being. his paper describes the protocol for a randomized controlled trial whose objective is to evaluate the Thrive program in comparison with an active control condition to measure whether the program is effective at increasing well-being and decreasing symptoms of psychological distress in health care workers at a designated Australian hospital. he trial will comprise two groups (intervention vs active control) and 4 measurement occasions over a 12-week period. A survey will be administered in each of weeks 0, 4, 8, and 12, and the well-being program will be delivered in weeks 1-7 (via web-based video presentations or digital p hlets). Each of the 4 surveys will comprise a range of questionnaires to measure well-being, psychological distress, and other key variables. The planned analyses will estimate group-by-time interaction effects to test the hypothesis that mental health will increase over time in the intervention condition relative to the active control condition. he Thrive program was delivered to a small number of wards at the hospital between February 2021 and July 2021, and it will be delivered to the remaining wards from October 2021 to December 2021. A power calculation has recommended a s le size of at least 200 participants in total. A linear mixed model will be used to estimate the interaction effects. his trial seeks to evaluate a new web-based well-being program for health care workers at a major public hospital. It will contribute to the growing body of research on mental well-being and ways to promote it. ustralian New Zealand Clinical Trials Registry ACTRN12621000027819 8wwjut9 ERR1-10.2196/34005
Publisher: Elsevier BV
Date: 02-2009
DOI: 10.1016/J.BIOPSYCHO.2008.09.001
Abstract: In this study, we examined whether the Met allele of the BDNF Val66Met polymorphism is associated with selective disruptions to task-relevant information processing. In 475 non-clinical participants for whom BDNF genotype status was determined we used the 'IntegNeuro' computerized battery of neuropsychological tests to assess cognitive performance, an auditory oddball task to elicit the P300 event-related potential (ERP) and, in smaller subsets of these subjects, high resolution structural MRI imaging to quantify fronto-hippoc al grey matter (n=161), and functional magnetic resonance imaging to assess fronto-hippoc al BOLD activation (n=37). Met/Met (MM) homozygotes had higher verbal recall errors, in the absence of differences in attention, executive function, verbal ability or sensori-motor function. Further, MM homozygotes demonstrated a slowed P300 ERP during the oddball task, with corresponding alterations in hippoc al and lateral prefrontal activation, and a localized reduction in hippoc al grey matter. These results are consistent with a subtle impact of the Met allele on fronto-hippoc al systems involved in selective information processing of stimulus context and memory updating within the normal population. The findings also indicate that heritable endophenotypes such as the P300 have value in elucidating genotype-phenotype relationships.
Publisher: World Scientific Pub Co Pte Lt
Date: 03-2007
DOI: 10.1142/S0219635207001465
Abstract: There is little consensus about which objective markers should be used to assess major psychiatric disorders, and predict/evaluate treatment response for these disorders. Clinical practice relies instead on subjective signs and symptoms, such that there is a "translational gap" between research findings and clinical practice. This gap arises from: a) a lack of integrative theoretical models which provide a basis for understanding links between gene-brain-behavior mechanisms and clinical entities b) the reliance on studying one measure at a time so that linkages between markers are their specificity are not established and c) the lack of a definitive understanding of what constitutes normative function. Here, we draw on a standardized methodology for acquiring multiple sources of genomic, brain and behavioral data in the same subjects, to propose candidate markers of selected psychiatric disorders: depression, post-traumatic stress disorder, schizophrenia, attention-deficit/hyperactivity disorder and dementia disorders. This methodology has been used to establish a standardized international database which provides a comprehensive framework and the basis for testing hypotheses derived from an integrative theoretical model of the brain. Using this normative base, we present preliminary findings for a number of disorders in relation to the proposed markers. Establishing these objective markers will be the first step towards determining their sensitivity, specificity and treatment prediction in in idual patients.
Publisher: SAGE Publications
Date: 30-08-2018
Abstract: The sequelae of migration and the effects of local migration policies on children’s physical and mental health are critical to examine, particularly given the historically high numbers of migrants and displaced people. The vulnerability of the study s le and the need to work across cultures and contexts makes research on this group challenging. We outline lessons learned through conducting a pilot study of resilience resources and mental health among migrant youth in six countries. We describe the benefits and challenges, and then provide recommendations and practical advice for social work researchers attempting cross-cultural team research on migrants.
Publisher: Elsevier BV
Date: 07-2016
DOI: 10.1016/J.JPSYCHIRES.2016.03.006
Abstract: Enhanced threat-related processing is associated with both elevated anxiety and childhood exposure to trauma. Given the paucity of evidence regarding the effects of childhood and adult trauma exposure on subsequent psychophysiological processes in the absence of psychopathology, we investigated the relative impacts of childhood interpersonal and non-interpersonal trauma, as well as adult trauma exposure on neural processing of threat in healthy adults. We measured peak litudes of the N170 face-sensitive visual ERP component response to non-conscious and conscious Angry (threat) versus Happy (non-threat, positive) and Neutral (non-threat baseline) faces at temporo-occipital sites (right-T6 left-T5) in 489 psychiatrically asymptomatic adults (aged 18-70 years, 54% women, 94% right-handed). N170 peak litude differences between Angry vs Happy or Neutral faces were calculated and subjected to hierarchical multiple regression analysis, with trauma types (childhood interpersonal, childhood non-interpersonal and adult trauma) entered as predictors of interest. After controlling for sociodemographic and health factors, N170 peak litudes for non-conscious Angry vs Happy faces were inversely associated with childhood interpersonal trauma at T6 and adult trauma exposure at T5. Post-hoc repeated measures ANOVA indicated that unlike adults without trauma exposure, trauma-exposed adults failed to show significantly reduced N170 responses to Happy relative to Angry faces during non-conscious processing. This suggests that childhood interpersonal and adult trauma exposure are associated with a failure to differentiate between non-threat or positive and threat-related emotion cues. This is consistent with generalised hypervigilance seen in PTSD, and suggests trauma exposure is associated with a generalized heightened responsivity to non-conscious non-threat or positive as well as threat-related emotion cues in psychiatrically healthy adults.
Publisher: BMJ
Date: 07-2022
DOI: 10.1136/BMJOPEN-2021-058918
Abstract: Mental well-being is a core component of mental health, and resilience is a key process of positive adaptive recovery following adversity. However, we lack an understanding of the neural mechanisms that contribute to in idual variation in the trajectories of well-being and resilience relative to risk. Genetic and/or environmental factors may also modulate these mechanisms. The aim of the TWIN-10 Study is to characterise the trajectories of well-being and resilience over 12 years across four timepoints (baseline, 1 year, 10 years, 12 years) in 1669 Australian adult twins of European ancestry (to account for genetic stratification effects). To this end, we integrate data across genetics, environment, psychological self-report, neurocognitive performance and brain function measures of well-being and resilience. Twins who took part in the baseline TWIN-E Study will be invited back to participate in the TWIN-10 Study, at 10-year and 12-year follow-up timepoints. Participants will complete an online battery of psychological self-reports, computerised behavioural assessments of neurocognitive functions and MRI testing of the brain structure and function during resting and task-evoked scans. These measures will be used as predictors of the risk versus resilience trajectory groups defined by their changing levels of well-being and illness symptoms over time as a function of trauma exposure. Structural equation models will be used to examine the association between the predictors and trajectory groups of resilience and risk over time. Univariate and multivariate twin modelling will be used to determine heritability of the measures, as well as the shared versus unique genetic and environmental contributions. This study involves human participants. This study was approved by the University of New South Wales Human Research Ethics Committee (HC180403) and the Scientific Management Panel of Neuroscience Research Australia Imaging (CX2019-05). Results will be disseminated through publications and presentations to the public and the academic community. Participants gave informed consent to participate in the study before taking part.
Publisher: Wiley
Date: 22-01-2014
DOI: 10.1002/HBM.22446
Publisher: Elsevier BV
Date: 2015
DOI: 10.1016/J.JPSYCHIRES.2014.09.014
Abstract: Major efforts have been directed at family-based association and case-control studies to identify the involvement of candidate genes in the major disorders of mental health. What remains unknown is whether candidate genes are associated with multiple disorders via pleiotropic mechanisms, and/or if other genes are specific to susceptibility for in idual disorders. Here we undertook a review of genes that have been identified in prior meta-analyses examining specific genes and specific mental disorders that have core disruptions to emotional and cognitive function and contribute most to burden of illness- major depressive disorder (MDD), anxiety disorders (AD, including panic disorder and obsessive compulsive disorder), schizophrenia (SZ) and bipolar disorder (BD) and attention deficit hyperactivity disorder (ADHD). A literature review was conducted up to end-March 2013 which included a total of 1519 meta-analyses across 157 studies reporting multiple genes implicated in one or more of the five disorders studied. A total of 134 genes (206 variants) were identified as significantly associated risk variants for MDD, AD, ADHD, SZ or BD. Null genetic effects were also reported for 195 genes (426 variants). 13 genetic variants were shared in common between two or more disorders (APOE e4, ACE Ins/Del, BDNF Val66Met, COMT Val158Met, DAOA G72/G30 rs3918342, DAT1 40-bp, DRD4 48-bp, SLC6A4 5-HTTLPR, HTR1A C1019G, MTHR C677T, MTHR A1298C, SLC6A4 VNTR and TPH1 218A/C) demonstrating evidence for pleiotrophy. Another 12 meta-analyses of GWAS studies of the same disorders were identified, with no overlap in genetic variants reported. This review highlights the progress that is being made in identifying shared and unique genetic mechanisms that contribute to the risk of developing several major psychiatric disorders, and identifies further steps for progress.
Publisher: Elsevier BV
Date: 11-2010
DOI: 10.1016/J.NEUROIMAGE.2010.01.084
Abstract: Biases toward processing negative versus positive information vary as a function of level of awareness, and are modulated by monoamines. Excessive biases are associated with in idual differences in mood and emotional stability, and emotional disorder. Here, we examined the impact of the catechol-O-methyltransferase (COMT) Val(108/158)Met polymorphism, involved in dopamine and norepinephrine catabolism, on both emotional brain function and self-reported negativity bias. COMT genotyping and self-reported level of negativity bias were completed for 46 healthy participants taking part in the Brain Resource International Database. Functional MRI was undertaken during perception of facial expressions of fear and happiness presented under unmasked (consciously identified) and masked (to prevent conscious detection) conditions. Structural MR images were also acquired. A greater number of COMT Met alleles predicted increased activation in brainstem, amygdala, basal ganglia and medial prefrontal regions for conscious fear, but decreased activation for conscious happiness. This pattern was also apparent for brainstem activation for the masked condition. Effects were most apparent for females. These differences could not be explained by gray matter variations. The Met-related profile of activation, particularly prefrontally, predicted greater negativity bias associated with risk for emotional disorder. The findings suggest that the COMT Met allele modulates neural substrates of negative versus positive emotion processing. This effect may contribute to negativity biases, which confer susceptibility for emotional disorders.
Publisher: Elsevier BV
Date: 12-2015
DOI: 10.1016/J.JAD.2015.08.053
Abstract: The prevalence of depression and anxiety symptoms and their comorbidity varies between males and females for reasons still unknown. This study aims to test whether differences between males and females in self-reported symptoms and their covariation are caused by variations in the magnitude of genetic and environmental factors. 750 monozygotic and dizygotic healthy twin pairs (18-60 years M=39.77 years) participated in the TWIN-E project. Univariate and multivariate genetic modelling was undertaken using the Depression Anxiety Stress Scale (DASS-42). Additive genetics and unique environment contributed to self-reported depression (heritability, h(2): 34%), anxiety (h(2): 30%) and stress (h(2): 34%) scores in univariate models, and to the common latent factor (h(2): 39%) in the multivariate model. No sex differences in magnitude of estimates for DASS-42 scores were found in the univariate model. However when considering correlated depression and anxiety symptomatology only shared genetic factors between depression and anxiety contributed to depression scores in males, but both specific and shared genetic factors contributed to depression scores in females. The results are limited to the s le of healthy, community, adult, same sex twin pairs who participated in the study. Differences in males and females in genetic aetiology of self-reported dimensions of depression are only apparent when taking into consideration the covariation with self-reported anxiety. This difference is highlighted by the finding that both common and specific genetic factors contribute to self-reported depression in females but not males. This novel finding may help explain the increased incidence of depression symptoms in females.
Publisher: Wiley
Date: 29-06-2022
DOI: 10.1002/HBM.25993
Abstract: Wellbeing, an important component of mental health, is influenced by genetic and environmental factors. Previous association studies between brain structure and wellbeing have typically focused on volumetric measures and employed small cohorts. Using the UK Biobank Resource, we explored the relationships between wellbeing and brain morphometrics (volume, thickness and surface area) at both phenotypic and genetic levels. The s le comprised 38,982 participants with neuroimaging and wellbeing phenotype data, of which 19,234 had genotypes from which wellbeing polygenic scores (PGS) were calculated. We examined the association of wellbeing phenotype and PGS with all brain regions (including cortical, subcortical, brainstem and cerebellar regions) using multiple linear models, including (1) basic neuroimaging covariates and (2) additional demographic factors that may synergistically impact wellbeing and its neural correlates. Genetic correlations between genomic variants influencing wellbeing and brain structure were also investigated. Small but significant associations between wellbeing and volumes of several cerebellar structures ( β = 0.015–0.029, P FDR = 0.007–3.8 × 10 −9 ), brainstem, nucleus accumbens and caudate were found. Cortical associations with wellbeing included volume of right lateral occipital, thickness of bilateral lateral occipital and cuneus, and surface area of left superior parietal, supramarginal and pre‐ ost‐central regions. Wellbeing‐PGS was associated with cerebellar volumes and supramarginal surface area. Small mediation effects of wellbeing phenotype and PGS on right VIIIb cerebellum were evident. No genetic correlation was found between wellbeing and brain morphometric measures. We provide a comprehensive overview of wellbeing‐related brain morphometric variation. Notably, small effect sizes reflect the multifaceted nature of this concept.
Start Date: 2008
End Date: 2011
Funder: Australian Research Council
View Funded ActivityStart Date: 05-2009
End Date: 05-2013
Amount: $670,000.00
Funder: Australian Research Council
View Funded Activity