ORCID Profile
0000-0003-4532-8571
Current Organisation
University of Cambridge
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Political Theory and Political Philosophy | Political theory and political philosophy | Comparative Government and Politics | Australian Government and Politics | Political Science | Comparative government and politics | Political science
Civics and Citizenship | Visual Communication | Political Systems |
Publisher: Springer Science and Business Media LLC
Date: 02-06-2022
DOI: 10.1038/S41588-022-01072-5
Abstract: The substantial phenotypic heterogeneity in autism limits our understanding of its genetic etiology. To address this gap, here we investigated genetic differences between autistic in iduals ( n max = 12,893) based on core and associated features of autism, co-occurring developmental disabilities and sex. We conducted a comprehensive factor analysis of core autism features in autistic in iduals and identified six factors. Common genetic variants were associated with the core factors, but de novo variants were not. We found that higher autism polygenic scores (PGS) were associated with lower likelihood of co-occurring developmental disabilities in autistic in iduals. Furthermore, in autistic in iduals without co-occurring intellectual disability (ID), autism PGS are overinherited by autistic females compared to males. Finally, we observed higher SNP heritability for autistic males and for autistic in iduals without ID. Deeper phenotypic characterization will be critical in determining how the complex underlying genetics shape cognition, behavior and co-occurring conditions in autism.
Publisher: Springer Science and Business Media LLC
Date: 12-07-2023
DOI: 10.1057/S41269-022-00253-8
Abstract: Nativism is one of the defining phenomena of the contemporary era. Yet, we know little about how malleable citizen attitudes associated with nativism and nationalism are to priming effects when media frames which deal with key issues such as immigration are introduced. In this article, we present the findings from a survey experiment fielded to a nationally representative s le of voters in Australia in May 2019. In it, we explore whether the attitudes of voters for different political parties can be primed by introducing two contrasting media frames to measure these effects. We find positive and negative frames have no effect on the attitudes of voters for Australia’s populist radical right party, but that the former has an effect on centre-right voters in Australia. Such findings have important implications for our understanding of political communication and the malleability of political attitudes.
Publisher: Cold Spring Harbor Laboratory
Date: 21-03-2022
DOI: 10.1101/2022.03.19.22272444
Abstract: Higher educational attainment is observationally associated with lower risk of Alzheimer’s disease. However, the biological mechanisms underpinning this association remain unclear. The protective effect of education on Alzheimer’s disease may be mediated via increased brain reserve. We used two-s le Mendelian randomization to explore putative causal relationships between educational attainment, structural brain reserve as proxied by MRI phenotypes, and Alzheimer’s disease. Summary statistics were obtained from genome-wide association studies of educational attainment ( n =1,131,881), late-onset Alzheimer’s disease (35,274 cases, 59,163 controls), and 15 measures of grey or white matter macro- or micro-structure derived from structural or diffusion MRI ( n max =33,211). We conducted univariable Mendelian randomization analyses to investigate bidirectional associations between (i) educational attainment and Alzheimer’s disease, (ii) educational attainment and imaging-derived phenotypes, (iii) imaging-derived phenotypes and Alzheimer’s disease. Multivariable Mendelian randomization was used to assess whether brain structure phenotypes mediated the protective effect of education on Alzheimer’s disease risk. Genetically-proxied educational attainment was inversely associated with Alzheimer’s disease (odds ratio per standard deviation increase in genetically-predicted years of schooling = 0.70, 95% confidence interval [CI]: 0.60, 0.80). There was also evidence for positive associations between genetically-predicted educational attainment and four cortical macro-structure metrics (surface area: β=0.30, 95% CI: 0.20, 0.40 volume: β=0.29, 95% CI: 0.20, 0.37 intrinsic curvature: β=0.18, 95% CI: 0.11, 0.25 local gyrification index: β=0.21, 95% CI: 0.11, 0.31), as well as inverse associations with cortical intracellular volume fraction (β=-0.09, 95% CI: − 0.15, −0.03) and white matter hyperintensities volume (β=-0.14, 95% CI: −0.23, −0.05). Genetically-proxied levels of three cortical macro-structure metrics were positively associated with years of education (surface area: β=0.13, 95% CI: 0.10, 0.16 volume: β=0.15, 95% CI: 0.11, 0.19 intrinsic curvature: β=0.12, 95% CI: 0.04, 0.19). We found no evidence of associations between genetically-predicted imaging-derived phenotypes and Alzheimer’s disease. The inverse association of genetically-predicted education with Alzheimer’s disease did not attenuate after adjusting for imaging-derived phenotypes in multivariable analyses. Our results provide support for a protective causal effect of educational attainment on Alzheimer’s disease risk, as well as bi-directional causal associations between education and several brain macro- and micro-structure metrics. However, we did not find evidence that these structural markers affect risk of Alzheimer’s disease. The protective effect of education on Alzheimer’s disease may be mediated via other measures of brain reserve not included in the present study, or by alternative mechanisms.
Publisher: SAGE Publications
Date: 24-03-2021
Abstract: The study of populist attitudes has thus far drawn heavily on ideational definitions of populism, focussing almost exclusively on attitudes related to dimensions such as people-centredness and anti-elitism. However, these accounts have largely ignored other approaches to populism, especially the discursive-performative school which see populism as something that is communicated and done by political actors. We argue that when studying populist attitudes, these approaches are not mutually exclusive. In this article, we develop a novel measure of attitudes towards populist communication and consider how these interact with populist ideational attitudes. Testing our measures on the Australian case, we demonstrate that attitudes towards populist communication exist independently of populist ideational attitudes, and that they have a significant effect on voting behaviour and on attitudes related to the ideational approach. Therefore, we argue that studies of populist attitudes need to take attitudes towards populist communication into account in future work.
Publisher: John Benjamins Publishing Company
Date: 09-05-2023
Abstract: This article examines one of the longest-standing populist radical right parties outside of Europe: Pauline Hanson’s One Nation. The article outlines the party’s development and position in the Australian political landscape, before explaining how it articulates the ideological features of the PRR (nativism, authoritarianism and populism) how these interact and in what ways this differs from European PRR parties. It shows that the party has steadfastly remained focused on targeting outgroups – immigrants, asylum seekers, Asians, Muslims, and First Nations Peoples, amongst others – rather than clearly defining its ingroup – ‘ordinary Australians’ – and considers the role of Australia’s settler-colonial history and geographical context in this. It then analyses how the party has broadened its platform in recent years by engaging with gender identity, vaccine mandates, climate change scepticism and sovereign-citizen issues before explaining the factors that have prevented it from achieving the success of many European PRR parties.
Publisher: Springer Science and Business Media LLC
Date: 30-08-2021
DOI: 10.1038/S41380-021-01260-5
Abstract: Recent discovery of approximately 270 common genetic variants associated with schizophrenia has enabled polygenic risk scores (PRS) to be measured in the population. We hypothesized that normal variation in PRS would be associated with magnetic resonance imaging (MRI) phenotypes of brain morphometry and tissue composition. We used the largest extant genome-wide association dataset ( N = 69,369 cases and N = 236,642 healthy controls) to measure PRS for schizophrenia in a large s le of adults from the UK Biobank ( N max = 29,878) who had multiple micro- and macrostructural MRI metrics measured at each of 180 cortical areas, seven subcortical structures, and 15 major white matter tracts. Linear mixed-effect models were used to investigate associations between PRS and brain structure at global and regional scales, controlled for multiple comparisons. Polygenic risk was significantly associated with reduced neurite density index (NDI) at global brain scale, at 149 cortical regions, five subcortical structures, and 14 white matter tracts. Other microstructural parameters, e.g., fractional anisotropy, that were correlated with NDI were also significantly associated with PRS. Genetic effects on multiple MRI phenotypes were co-located in temporal, cingulate, and prefrontal cortical areas, insula, and hippoc us. Post-hoc bidirectional Mendelian randomization analyses provided preliminary evidence in support of a causal relationship between (reduced) thalamic NDI and (increased) risk of schizophrenia. Risk-related reduction in NDI is plausibly indicative of reduced density of myelinated axons and dendritic arborization in large-scale cortico-subcortical networks. Cortical, subcortical, and white matter microstructure may be linked to the genetic mechanisms of schizophrenia.
Publisher: Cold Spring Harbor Laboratory
Date: 08-02-2021
DOI: 10.1101/2021.02.04.21251136
Abstract: Smoking, inflammation and depression commonly co-occur and may be mechanistically linked. However, key questions remain around the direction of association and the influence of residual confounding. We aimed to characterize the association between lifetime smoking and depression, as well as to assess the role that genetically-predicted C-reactive protein (CRP) level, an archetypal inflammatory marker, as a potential mediator for this association. We performed inverse variance weighted Mendelian randomization (MR) analyses using recently published summary-level GWAS data for lifetime smoking index, CRP levels, and depression. A subset of inflammatory-related genetic variants from the lifetime smoking GWAS were also used to assess the potential inflammatory causal pathways between smoking and depression. The analysis indicated significant reciprocal relationships between lifetime smoking and both depression (OR Smk-Dep = 2.01, 95% CI 1.71-2.37, p 0.001 O R Dep-Smk = 1.09, 95% CI 1.06-1.13, p 0.001) and CRP levels (OR Smk-CRP = 1.40, 95% CI 1.21-1.55, p 0.001 OR CRP-Smk = 1.03, 95% CI 1.02-1.05, p 0.001). These significant and positive associations were also supported by the majority of the robust MR methods performed. The reciprocal relationships between CRP levels (using genetic instruments for CRP) and depression were not significant (OR CRP-Dep = 1.01, 95% CI 0.99-1.04 OR Dep-CRP = 1.03, 95% CI 0.99-1.07). We observed little variation in the IVW estimates between smoking and depression when we limited the genetic variants assessed to those related to inflammation or when we adjusted the analysis by CRP-levels in multivariable analysis. Our study supports potential causal associations between lifetime smoking and depression, as well as between lifetime smoking and CRP levels, but not between CRP and depression. No evidence was found that CRP mediates the relationship between smoking and depression.
Publisher: Springer Science and Business Media LLC
Date: 17-08-2023
Publisher: Springer Science and Business Media LLC
Date: 26-06-2023
DOI: 10.1038/S41591-023-02408-2
Abstract: While over 100 genes have been associated with autism, little is known about the prevalence of variants affecting them in in iduals without a diagnosis of autism. Nor do we fully appreciate the phenotypic ersity beyond the formal autism diagnosis. Based on data from more than 13,000 in iduals with autism and 210,000 undiagnosed in iduals, we estimated the odds ratios for autism associated to rare loss-of-function (LoF) variants in 185 genes associated with autism, alongside 2,492 genes displaying intolerance to LoF variants. In contrast to autism-centric approaches, we investigated the correlates of these variants in in iduals without a diagnosis of autism. We show that these variants are associated with a small but significant decrease in fluid intelligence, qualification level and income and an increase in metrics related to material deprivation. These effects were larger for autism-associated genes than in other LoF-intolerant genes. Using brain imaging data from 21,040 in iduals from the UK Biobank, we could not detect significant differences in the overall brain anatomy between LoF carriers and non-carriers. Our results highlight the importance of studying the effect of the genetic variants beyond categorical diagnosis and the need for more research to understand the association between these variants and sociodemographic factors, to best support in iduals carrying these variants.
Publisher: Cold Spring Harbor Laboratory
Date: 08-02-2021
DOI: 10.1101/2021.02.06.21251073
Abstract: Recent discovery of approximately 270 common genetic variants associated with schizophrenia has enabled polygenic risk scores (PRS) to be measured in the population. We hypothesized that normal variation in PRS would be associated with magnetic resonance imaging (MRI) phenotypes of brain morphometry and tissue composition. We used the largest extant genome-wide association dataset (N = 69,369 cases and N = 236,642 healthy controls) to measure PRS for schizophrenia in a large s le of adults from the UK Biobank (Nmax = 29,878) who had multiple micro- and macro-structural MRI metrics measured at each of 180 cortical areas, seven subcortical structures, and 15 major white matter tracts. Linear mixed effect models were used to investigate associations between PRS and brain structure at global and regional scales, controlled for multiple comparisons. Polygenic risk was significantly associated with reduced neurite density index (NDI) at global brain scale, at 149 cortical regions, five subcortical structures and 14 white matter tracts. Other micro-structural parameters, e.g., fractional anisotropy, that were correlated with NDI were also significantly associated with PRS. Genetic effects on multiple MRI phenotypes were co-located in temporal, cingulate and prefrontal cortical areas, insula, and hippoc us. Post-hoc bidirectional Mendelian randomization analyses provided preliminary evidence in support of a causal relationship between (reduced) thalamic NDI and (increased) risk of schizophrenia. Risk-related reduction in NDI is plausibly indicative of reduced density of myelinated axons and dendritic arborization in large-scale cortico-subcortical networks. Cortical, subcortical and white matter micro-structure may be linked to the genetic mechanisms of schizophrenia.
Publisher: Informa UK Limited
Date: 10-2023
Publisher: Cold Spring Harbor Laboratory
Date: 08-09-2022
DOI: 10.1101/2022.09.08.507084
Abstract: Our understanding of the genetic architecture of the human cerebral cortex is limited both in terms of the ersity of brain structural phenotypes and the anatomical granularity of their associations with genetic variants. Here, we conducted genome-wide association meta-analysis of 13 structural and diffusion magnetic resonance imaging derived cortical phenotypes, measured globally and at 180 bilaterally averaged regions in 36,843 in iduals from the UK Biobank and the ABCD cohorts. These phenotypes include cortical thickness, surface area, grey matter volume, and measures of folding, neurite density, and water diffusion. We identified 4,349 experiment-wide significant loci associated with global and regional phenotypes. Multiple lines of analyses identified four genetic latent structures and causal relationships between surface area and some measures of cortical folding. These latent structures partly relate to different underlying gene expression trajectories during development and are enriched for different cell types. We also identified differential enrichment for neurodevelopmental and constrained genes and demonstrate that common genetic variants associated with surface area and volume specifically are associated with cephalic disorders. Finally, we identified complex inter-phenotype and inter-regional genetic relationships among the 13 phenotypes which reflect developmental differences among them. These analyses help refine the role of common genetic variants in human cortical development and organisation. GWAS of 2,347 neuroimaging phenotypes shed light on the global and regional genetic organisation of the cortex, underlying cellular and developmental processes, and links to neurodevelopmental and cephalic disorders.
Publisher: Springer Science and Business Media LLC
Date: 06-06-2018
DOI: 10.1038/MP.2017.122
Location: United Kingdom of Great Britain and Northern Ireland
Start Date: 07-2024
End Date: 06-2027
Amount: $312,265.00
Funder: Australian Research Council
View Funded ActivityStart Date: 12-2019
End Date: 12-2024
Amount: $379,000.00
Funder: Australian Research Council
View Funded Activity