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Murray, G. K.

Publications and source records attributed to Murray, G. K..

10 recordsLinked to original sources

The complementary roles of rare variant burden scores and common variant polygenic risk scores in genetic risk prediction of complex disorders

Polygenic risk scores (PRS) derived from common variants have improved risk prediction for complex disorders, however they capture only a fraction of heritability. One of the reasons for this is the exclusion of rare variants, despite growing evidence of their substantial contribution to genetic liability. Here we implemented the Independent Outlier Gene Count (IOGC) - a score summarising the individual burden of rare variants associated with outlying gene expression - and measured the amount of liability explained by this rare-variant score, alone and in combination with common-variant PRS, for schizophrenia, major depressive disorder, and hypertrophic cardiomyopathy in the UK Biobank. IOGC and PRS were minimally correlated (|r|<0.2), indicating the two scores capture complementary information. For schizophrenia, a model including both IOGC and PRS explained 1.13 times the adjusted liability than PRS alone. For hypertrophic cardiomyopathy, a 1.48-fold increase was observed for the combined model. People with high IOGC showed a 64% and 46% higher positive predictive value for schizophrenia and HCM, respectively, as compared to those with low IOGC. No improvement was observed for depression. These findings demonstrate that integrating rare- and common-variant scores enhances genetic risk prediction for complex conditions with a strong genetic component, supporting the inclusion of rare variant burden metrics in future genomic risk models.

genomics↗

The genetics of cortical organisation and development: a study of 2,347 neuroimaging phenotypes

Our understanding of the genetic architecture of the human cerebral cortex is limited both in terms of the diversity 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 individuals 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. One sentence summaryGWAS 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.

neuroscience↗

Genome-wide association study of gastrointestinal disorders reinforces the link between the digestive tract and the nervous system

Genetic factors are recognized to contribute to common gastrointestinal (GI) diseases such as gastro-oesophageal reflux disease (GORD), peptic ulcer disease (PUD), irritable bowel syndrome (IBS) and inflammatory bowel disease (IBD). We conducted genome-wide association analyses based on 456,414 individuals and identified 27 independent and significant loci for GORD, PUD and IBS, including SNPs associated with PUD at or near genes MUC1, FUT2, PSCA and CCKBR, for which there are previously established roles in Helicobacter pylori infection, response to counteract infection-related damage, gastric acid secretion and gastrointestinal motility. Post-GWAS analyses implicate putative functional links between the nervous system and gastrointestinal tract for GORD, PUD and IBS, including the central nervous system, the enteric nervous system and their connection. Mendelian Randomisation analyses imply potentially bi-directional causality (the risk of GORD in liability to major depression and the risk of major depression in liability to GORD) or pleiotropic effect between them. A stronger genetic similarity among GORD, PUD and IBS than between these disorders and IBD is reported. These findings advance understanding the role of genetic variants in the etiology of GORD, PUD and IBS and add biological insights into the link between the nervous system and the gastrointestinal tract.

genomics↗

Reinforcement learning as an intermediate phenotype in psychosis? Deficits sensitive to illness stage but not associated with polygenic risk of schizophrenia in the general population

BackgroundSchizophrenia is a complex disorder in which the causal relations between risk genes and observed clinical symptoms are not well understood and the explanatory gap is too wide to be clarified without considering an intermediary level. Thus, we aimed to test the hypothesis of a pathway from molecular polygenic influence to clinical presentation occurring via deficits in reinforcement learning. MethodsWe administered a reinforcement learning task (Go/NoGo) that measures reinforcement learning and the effect of Pavlovian bias on decision making. We modelled the behavioural data with a hierarchical Bayesian approach (hBayesDM) to decompose task performance into its underlying learning mechanisms. Study 1 included controls (n= 29, F|M=0.81), At Risk Mental State for psychosis (ARMS, n= 23, F|M=0.35) and FEP (First-episode psychosis, n= 26, F|M=0.18). Study 2 included healthy adolescents (n= 735, F|M= 1.06), 390 of whom had their polygenic risk scores for schizophrenia (PRSs) calculated. ResultsPatients with FEP showed significant impairments in overriding Pavlovian conflict, a lower learning rate and a lower sensitivity to both reward and punishment. Less widespread deficits were observed in ARMS. PRSs did not significantly predict performance on the task in the general population, which only partially correlated with measures of psychopathology. ConclusionsReinforcement learning deficits are observed in first episode psychosis and, to some extent, in those at clinical risk for psychosis, and were not predicted by molecular genetic risk for schizophrenia in healthy individuals. The study does not support the role of reinforcement learning as an intermediate phenotype in psychosis.

neuroscience↗

Novel genome-wide associations for anhedonia, genetic correlation with psychiatric disorders, and polygenic association with brain structure.

Anhedonia is a core feature of several psychiatric disorders but its biological underpinnings are poorly understood. We performed a genome-wide association study of anhedonia in 375,275 UK Biobank participants and assessed for genetic correlation between anhedonia and neuropsychiatric conditions (major depressive disorder, schizophrenia, bipolar disorder, obsessive compulsive disorder and Parkinsons Disease). We then used a polygenic risk score approach to test for association between genetic loading for anhedonia and both brain structure and brain function. This included: magnetic resonance imaging (MRI) assessments of total grey matter volume, white matter volume, cerebrospinal fluid volume, and 15 cortical/subcortical regions of interest; diffusion tensor imaging (DTI) measures of white matter tract integrity; and functional MRI activity during an emotion processing task. We identified 11 novel loci associated at genome-wide significance with anhedonia, with a SNP heritability estimate (h2SNP) of 5.6%. Strong positive genetic correlations were found between anhedonia and major depressive disorder, schizophrenia and bipolar disorder; but not with obsessive compulsive disorder or Parkinsons Disease. Polygenic risk for anhedonia was associated with poorer brain white matter integrity, smaller total grey matter volume, and smaller volumes of brain regions linked to reward and pleasure processing, including nucleus accumbens, caudate and medial frontal cortex. In summary, the identification of novel anhedonia-associated loci substantially expands our current understanding of the biological basis of anhedonia and genetic correlations with several psychiatric disorders confirm the utility of this trait as a transdiagnostic marker of vulnerability to mental illness. We also provide the first evidence that genetic risk for anhedonia influences brain structure, particularly in regions associated with reward and pleasure processing.

genetics↗

Jumping To Conclusions, General Intelligence, And Psychosis Liability: Findings From The Multicentric EU-GEI Case-Control Study

BackgroundThe \"jumping to conclusions\" (JTC) bias is associated with both psychosis and general cognition but their relationship is unclear. In this study, we set out to clarify the relationship between the JTC bias, IQ, psychosis and polygenic liability to schizophrenia and IQ.\n\nMethods817 FEP patients and 1294 population-based controls completed assessments of general intelligence (IQ), and JTC (assessed by the number of beads drawn on the probabilistic reasoning \"beads\" task) and provided blood or saliva samples from which we extracted DNA and computed polygenic risk scores for IQ and schizophrenia.\n\nResultsThe estimated proportion of the total effect of case/control differences on JTC mediated by IQ was 79%. Schizophrenia Polygenic Risk Score (SZ PRS) was non-significantly associated with a higher number of beads drawn (B= 0.47, 95% CI -0.21 to 1.16, p=0.17); whereas IQ PRS (B=0.51, 95% CI 0.25 to 0.76, p<0.001) significantly predicted the number of beads drawn, and was thus associated with reduced JTC bias. The JTC was more strongly associated with higher level of psychotic-like experiences (PLE) in controls, including after controlling for IQ (B= -1.7, 95% CI -2.8 to -0.5, p=0.006), but did not relate to delusions in patients.\n\nConclusionsthe JTC reasoning bias in psychosis is not a specific cognitive deficit but is rather a manifestation or consequence, of general cognitive impairment. Whereas, in the general population, the JTC bias is related to psychotic-like experiences, independent of IQ. The work has potential to inform interventions targeting cognitive biases in early psychosis.

neuroscience↗

Neural correlates of reward anticipation in 2000 children aged 9-10 years: relation to psychotic-like experiences and depressive symptoms

BackgroundSchizophrenia spectrum disorders and depression have been associated with reductions in brain activation during reward anticipation. It is not known whether brain signals associated with reward anticipation relate to psychopathology dimensions of depression or schizophrenia in childhood prior to adolescence.\n\nMethodWe examined whether fMRI brain correlates of reward anticipation related to psychotic-like experiences and symptoms of depression, in 2129 children from the ABCD study aged 9-10 years.Psychotic-like experiences and depression were assessed using the Prodromal Questionnaire Brief Child version and the K-SADS. We fused regional MRI summary statistics for reward anticipation activation in the ABCD study data release 1.0 (contrast of expected large reward versus neutral expectation). Relations between brain activation and psychopathology were assessed using linear regressions in R for 82 brain regions, corrected for multiple comparisons for the number of regions using false discovery rate.\n\nResultsFrom several regressions, there was an isolated unilateral association between right parsorbitalis activation and psychotic-like experiences, but no other significant associations between brain activation and psychopathology.\n\nConclusionsIn 9-10 year old children, reward anticipation is not strongly related to psychotic-like experiences or depression. As previous evidence links depression and schizophrenia to reduced reward anticipation in adults and older adolescents, it appears likely that such associations develop over the adolescent period: this can be tested in follow-up studies of the ABCD cohort.

neuroscience↗

Precision weighting of cortical unsigned prediction errors is mediated by dopamine and benefits learning

The predictive coding framework construes the brain as performing a specific form of hierarchical Bayesian inference. In this framework the precision of cortical unsigned prediction error (surprise) signals is proposed to play a key role in learning and decision-making, and to be controlled by dopamine. To test this hypothesis, we re-analysed an existing data-set from healthy individuals who received a dopamine agonist, antagonist or placebo and who performed an associative learning task under different levels of outcome precision. Computational reinforcement-learning modelling of behaviour provided support for precision-weighting of unsigned prediction errors. Functional MRI revealed coding of unsigned prediction errors relative to their precision in bilateral superior frontal gyri and dorsal anterior cingulate. Cortical precision-weighting was (i) perturbed by the dopamine antagonist sulpiride, and (ii) associated with task performance. These findings have important implications for understanding the role of dopamine in reinforcement learning and predictive coding in health and illness.

neuroscience↗

Dopaminergic drug treatment remediates exaggerated cingulate prediction error responses in obsessive-compulsive disorder

RationalePatients with obsessive-compulsive disorder (OCD) have been found to show exaggerated error responses and prediction error learning signals in a variety of EEG and fMRI tasks, with data converging on the anterior cingulate cortex as a key locus of dysfunction. Considerable evidence has linked prediction error processing to dopaminergic function.\n\nObjectiveIn this study we investigate potential dopaminergic dysfunction during reward processing in the context of OCD.\n\nMethodsWe studied OCD patients (n=18) and controls (n=18) whilst they learned probabilistic associations between abstract stimuli and monetary rewards in the fMRI scanner involving administration (on separate visits) of: a dopamine receptor agonist, pramipexole 0.5mg; a dopamine receptor antagonist, amisulpride 400mg, and placebo. We fitted a Q-learning computational model to fMRI prediction error responses; group differences were examined in anterior cingulate and nucleus accumbens regions of interest.\n\nResultsThere were no significant group, drug or interaction effects in number of correct choices; computational modeling suggested a marginally significant difference in learning rates between groups (p=0.089, partial 2=0.1). In the imaging results, there was a significant interaction of group by drug (p=0.013, partial 2=0.13). OCD patients showed abnormally strong cingulate signaling of prediction errors during omission of an expected reward, with unexpected reduction by both pramipexole and amisulpride (p=0.014, partial 2=0.26, 1-{beta} error probability=0.94). Exaggerated cingulate prediction error signaling to omitted reward in placebo was related to trait subjective difficulty in self-regulating behavior in OCD.\n\nConclusionsOur data support cingulate dysfunction during reward processing in OCD, and bidirectional remediation by dopaminergic modulation, suggesting that exaggerated cingulate error signals in OCD may be of dopaminergic origin. The results help to illuminate the mechanisms through which dopamine receptor antagonists achieve therapeutic benefit in OCD. Further research is needed to disentangle the different functions of dopamine receptor agonists and antagonists during bidirectional modulation of cingulate activation.

neuroscience↗

Abnormal reward prediction error signalling in antipsychotic naive individuals with first episode psychosis or clinical risk for psychosis

Ongoing research suggests preliminary, though not entirely consistent, evidence of neural abnormalities in signalling prediction errors in schizophrenia. Supporting theories suggest mechanistic links between the disruption of these processes and the generation of psychotic symptoms. However, it is not known at what stage in psychosis these impairments in prediction error signalling develop. One major confound in prior studies is the use of medicated patients with strongly varying disease durations. Our study aims to investigate the involvement of the meso-cortico-striatal circuitry during reward prediction error signalling in the earliest stages of psychosis. We studied patients with first episode psychosis (FEP) and help-seeking individuals at risk for psychosis due to subthreshold prodromal psychotic symptoms. Patients with either FEP (n = 14), or at-risk for developing psychosis (n= 30), and healthy volunteers (n = 39) performed a reinforcement learning task during fMRI scanning. ANOVA revealed significant (p<0.05 family-wise error corrected) prediction error signalling differences between groups in the dopaminergic midbrain and right middle frontal gyrus (dorsolateral prefrontal cortex, DLPFC). Patients with FEP showed disrupted reward prediction error signalling compared to controls in both regions. At-risk patients showed intermediate activation in the midbrain that significantly differed from controls and from FEP patients, but DLPFC activation that did not differ from controls. Our study confirms that patients with FEP have abnormal meso-cortical signalling of reward prediction errors, whilst reward prediction error dysfunction in the at-risk patients appears to show a more nuanced pattern of activation with a degree of midbrain impairment but preserved cortical function.

neuroscience↗