Queensland Center for Mental Health Research

Summer Hill, Australia

Queensland Center for Mental Health Research

Summer Hill, Australia
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Eyles D.W.,Queensland Center for Mental Health Research | Eyles D.W.,University of Queensland | Burne T.H.J.,Queensland Center for Mental Health Research | Burne T.H.J.,University of Queensland | And 2 more authors.
Frontiers in Neuroendocrinology | Year: 2013

Increasingly vitamin D deficiency is being associated with a number of psychiatric conditions. In particular for disorders with a developmental basis, such as autistic spectrum disorder and schizophrenia the neurobiological plausibility of this association is strengthened by the preclinical data indicating vitamin D deficiency in early life affects neuronal differentiation, axonal connectivity, dopamine ontogeny and brain structure and function. More recently epidemiological associations have been made between low vitamin D and psychiatric disorders not typically associated with abnormalities in brain development such as depression and Alzheimer's disease. Once again the preclinical findings revealing that vitamin D can regulate catecholamine levels and protect against specific Alzheimer-like pathology increase the plausibility of this link. In this review we have attempted to integrate this clinical epidemiology with potential vitamin D-mediated basic mechanisms. Throughout the review we have highlighted areas where we think future research should focus. © 2012.


Fan Y.,Griffith University | Abrahamsen G.,Griffith University | McGrath J.J.,Griffith University | McGrath J.J.,Queensland Center for Mental Health Research | And 2 more authors.
Biological Psychiatry | Year: 2012

The olfactory mucosa, the organ of smell in the nose, is a neural tissue that regenerates new sensory neurons throughout adult life. Based on this tissue, we previously demonstrated increased mitosis in olfactory biopsy cultures from schizophrenia patients compared with healthy control subjects. In addition, neural stem/progenitor cell cultures (neurosphere-derived cells) from nasal biopsies from individuals with schizophrenia show significantly altered gene and protein expression in key cell cycle control pathways. The aim of this study was to investigate cell cycle dynamics in olfactory neurosphere-derived cells from nine male schizophrenia patients and nine male healthy control subjects. Cell cycles were arrested by serum deprivation after which cell population doubling time, proliferation fraction, and cell cycle period were calculated from cell counts over 96 hours. Cell cycle phase was investigated using flow cytometry. Cell lysates were analyzed for expression of cyclin proteins. Cell population proliferation rate was increased in schizophrenia through a larger pool of proliferating progenitors and a reduced cell cycle period. All phases of the cell cycle were phase-shifted by 2 hours in the schizophrenia-derived cells, which expressed higher levels of the cyclins D1, E, and A2. Our observations indicate that schizophrenia is associated with subtle alterations in cell cycle dynamics, shortening of the cell cycle period, and increased expression of G1/S phase cyclins. We speculate that this underlying diathesis could alter the temporal and spatial cascade of brain development and contribute to an altered neurodevelopmental trajectory in schizophrenia. © 2012 Society of Biological Psychiatry.


Turner K.M.,University of Queensland | Burne T.H.J.,University of Queensland | Burne T.H.J.,Queensland Center for Mental Health Research
Frontiers in Behavioral Neuroscience | Year: 2013

Schizophrenia is associated with many genetic and environmental risk factors and there is growing evidence that the interactions between genetic and environmental 'hits' are critical for disease onset. Animal models of schizophrenia have traditionally used specific strain and housing conditions to test potential risk factors. As the field moves towards testing gene (G) x environment (E) interactions the impact of these choices should be considered. Given the surge of research focused on cognitive deficits, we have examined studies of cognition in rodents from the perspective of GxE interactions, in which strain or housing manipulations have been varied. Behaviour is clearly altered by these factors, yet few animal models of schizophrenia have investigated cognitive deficits using different strain and housing conditions. It is important to recognise the large variation in behaviour observed when using different strain and housing combinations because GxE interactions may mask or exacerbate cognitive outcomes. Further consideration will improve our understanding of GxE interactions and the underlying neurobiology of cognitive impairments in neuropsychiatric disorders. © 2013 Turner and Burne.


Norman R.E.,University of Queensland | Byambaa M.,University of Queensland | De R.,University of Queensland | Butchart A.,World Health Organization | And 4 more authors.
PLoS Medicine | Year: 2012

Background: Child sexual abuse is considered a modifiable risk factor for mental disorders across the life course. However the long-term consequences of other forms of child maltreatment have not yet been systematically examined. The aim of this study was to summarise the evidence relating to the possible relationship between child physical abuse, emotional abuse, and neglect, and subsequent mental and physical health outcomes. Methods and Findings: A systematic review was conducted using the Medline, EMBASE, and PsycINFO electronic databases up to 26 June 2012. Published cohort, cross-sectional, and case-control studies that examined non-sexual child maltreatment as a risk factor for loss of health were included. All meta-analyses were based on quality-effects models. Out of 285 articles assessed for eligibility, 124 studies satisfied the pre-determined inclusion criteria for meta-analysis. Statistically significant associations were observed between physical abuse, emotional abuse, and neglect and depressive disorders (physical abuse [odds ratio (OR) = 1.54; 95% CI 1.16-2.04], emotional abuse [OR = 3.06; 95% CI 2.43-3.85], and neglect [OR = 2.11; 95% CI 1.61-2.77]); drug use (physical abuse [OR = 1.92; 95% CI 1.67-2.20], emotional abuse [OR = 1.41; 95% CI 1.11-1.79], and neglect [OR = 1.36; 95% CI 1.21-1.54]); suicide attempts (physical abuse [OR = 3.40; 95% CI 2.17-5.32], emotional abuse [OR = 3.37; 95% CI 2.44-4.67], and neglect [OR = 1.95; 95% CI 1.13-3.37]); and sexually transmitted infections and risky sexual behaviour (physical abuse [OR = 1.78; 95% CI 1.50-2.10], emotional abuse [OR = 1.75; 95% CI 1.49-2.04], and neglect [OR = 1.57; 95% CI 1.39-1.78]). Evidence for causality was assessed using Bradford Hill criteria. While suggestive evidence exists for a relationship between maltreatment and chronic diseases and lifestyle risk factors, more research is required to confirm these relationships. Conclusions: This overview of the evidence suggests a causal relationship between non-sexual child maltreatment and a range of mental disorders, drug use, suicide attempts, sexually transmitted infections, and risky sexual behaviour. All forms of child maltreatment should be considered important risks to health with a sizeable impact on major contributors to the burden of disease in all parts of the world. The awareness of the serious long-term consequences of child maltreatment should encourage better identification of those at risk and the development of effective interventions to protect children from violence. Please see later in the article for the Editors' Summary. © 2012 Norman et al.


McGrath J.,Queensland Center for Mental Health Research | McGrath J.,University of Queensland | Brown A.,Columbia University | St Clair D.,University of Aberdeen
Schizophrenia Bulletin | Year: 2011

Adequate prenatal nutrition is essential for optimal brain development. There is a growing body of evidence from epidemiology linking exposure to nutritional deprivation and increased risk of schizophrenia. Based on studies from the Netherlands and China, those exposed to macronutrient deficiencies during famine have an increased risk of schizophrenia. With respect to micronutrients, we focus on 3 candidates where there is biological plausibility for a role in this disorder and at least 1 study of an association with schizophrenia. These nutrients include vitamin D, folic acid, and iron. While the current evidence is incomplete, we discuss the potential implications of these findings for the prevention of schizophrenia. We argue that schizophrenia can draw inspiration from public health interventions related to prenatal nutrition and other outcomes and speculate on relevant factors that bear on the nature, risks, impact, and logistics of various nutritional strategies that may be employed to prevent this disorder. © The Author 2011. Published by Oxford University Press on behalf of the Maryland Psychiatric Research Center. All rights reserved.


Nielsen R.E.,Aarhus University Hospital | Uggerby A.S.,Aarhus University Hospital | Jensen S.O.W.,Aarhus University Hospital | McGrath J.J.,Queensland Center for Mental Health Research | McGrath J.J.,University of Queensland
Schizophrenia Research | Year: 2013

Objective: The objective of this study is to describe secular trends in the average age of death in patients with schizophrenia and to compare these with the general population. Methods: This is a longitudinal linkage study from 1 January 1980 to 31 December 2010 using the Danish Psychiatric Research Register and the Danish Cause of Death Register. Data were analyzed using descriptive statistics and survival analysis. Results: The average age of death in the schizophrenia population (62.2. years; 95% CI, 61.9-62.5) was lower compared to the general population (73.4. years; 95% CI, 73.4-73.4), P< 0.001. In the general population we found, for men, an average increase in the age of death of 0.28. years (95% CI, 0.27-0.28) per calendar year, and for women an increase in age of death of 0.31. years (95% CI, 0.31-0.32) per calendar year (both P< 0.001). In contrast, age of death decreased in the schizophrenia population: the change in average age of death for males was 0.04. years (95% CI, - 0.09 to 0.00) per calendar year (P< 0.05), and the comparable estimate for females was - 0.05. years (95% CI, - 0.09 to 0.01) per calendar year (P< 0.05). A similar pattern existed after acts of self-harm as cause of death were excluded from the analyses. Patients diagnosed with schizophrenia had an increased mortality rate compared with the general population (hazard ratio, 2.05; 95% CI, 2.01-2.09). Conclusions: On average, patients with schizophrenia die younger than the general population, independent of intentional self-harm as cause of death. © 2013 Elsevier B.V.


Mowry B.J.,University of Queensland | Mowry B.J.,Queensland Center for Mental Health Research | Gratten J.,University of Queensland
Molecular Psychiatry | Year: 2013

After decades of halting progress, recent large genome-wide association studies (GWAS) are finally shining light on the genetic architecture of schizophrenia. The picture emerging is one of sobering complexity, involving large numbers of risk alleles across the entire allelic spectrum. The aims of this article are to summarize the key genetic findings to date and to compare and contrast methods for identifying additional risk alleles, including GWAS, targeted genotyping and sequencing. A further aim is to consider the challenges and opportunities involved in determining the functional basis of genetic associations, for instance using functional genomics, cellular models, animal models and imaging genetics. We conclude that diverse approaches will be required to identify and functionally characterize the full spectrum of risk variants for schizophrenia. These efforts should adhere to the stringent standards of statistical association developed for GWAS and are likely to entail very large sample sizes. Nonetheless, now more than any previous time, there are reasons for optimism and the ultimate goal of personalized interventions and therapeutics, although still distant, no longer seems unattainable. © 2013 Macmillan Publishers Limited.


Baxter A.J.,Queensland Center for Mental Health Research | Baxter A.J.,University of Queensland | Scott K.M.,University of Otago | Vos T.,University of Queensland | And 2 more authors.
Psychological Medicine | Year: 2013

Background The literature describing the global prevalence of anxiety disorders is highly variable. A systematic review and meta-regression were undertaken to estimate the prevalence of anxiety disorders and to identify factors that may influence these estimates. The findings will inform the new Global Burden of Disease study. Method A systematic review identified prevalence studies of anxiety disorders published between 1980 and 2009. Electronic databases, reference lists, review articles and monographs were searched and experts then contacted to identify missing studies. Substantive and methodological factors associated with inter-study variability were identified through meta-regression analyses and the global prevalence of anxiety disorders was calculated adjusting for study methodology. Results The prevalence of anxiety disorders was obtained from 87 studies across 44 countries. Estimates of current prevalence ranged between 0.9% and 28.3% and past-year prevalence between 2.4% and 29.8%. Substantive factors including gender, age, culture, conflict and economic status, and urbanicity accounted for the greatest proportion of variability. Methodological factors in the final multivariate model (prevalence period, number of disorders and diagnostic instrument) explained an additional 13% of variance between studies. The global current prevalence of anxiety disorders adjusted for methodological differences was 7.3% (4.8-10.9%) and ranged from 5.3% (3.5-8.1%) in African cultures to 10.4% (7.0-15.5%) in Euro/Anglo cultures. Conclusions Anxiety disorders are common and the substantive and methodological factors identified here explain much of the variability in prevalence estimates. Specific attention should be paid to cultural differences in responses to survey instruments for anxiety disorders. © 2012 Cambridge University Press.


Gratten J.,University of Queensland | Visscher P.M.,University of Queensland | Mowry B.J.,University of Queensland | Mowry B.J.,Queensland Center for Mental Health Research | Wray N.R.,University of Queensland
Nature Genetics | Year: 2013

Pedigree, linkage and association studies are consistent with heritable variation for complex disease due to the segregation of genetic factors in families and in the population. In contrast, de novo mutations make only minor contributions to heritability estimates for complex traits. Nonetheless, some de novo variants are known to be important in disease etiology. The identification of risk-conferring de novo variants will contribute to the discovery of etiologically relevant genes and pathways and may help in genetic counseling. There is considerable interest in the role of such mutations in complex neuropsychiatric disease, largely driven by new genotyping and sequencing technologies. An important role for large de novo copy number variations has been established. Recently, whole-exome sequencing has been used to extend the investigation of de novo variation to point mutations in protein-coding regions. Here, we consider several challenges for the interpretation of such mutations in the context of their role in neuropsychiatric disease. © 2013 Nature America, Inc. All rights reserved.


Groves N.J.,University of Queensland | McGrath J.J.,University of Queensland | McGrath J.J.,Queensland Center for Mental Health Research | Burne T.H.J.,University of Queensland | Burne T.H.J.,Queensland Center for Mental Health Research
Annual Review of Nutrition | Year: 2014

Vitamin D deficiency is prevalent throughout the world, and growing evidence supports a requirement for optimal vitamin D levels for the healthy developing and adult brain. Vitamin D has important roles in proliferation and differentiation, calcium signaling within the brain, and neurotrophic and neuroprotective actions; it may also alter neurotransmission and synaptic plasticity. Recent experimental studies highlight the impact that vitamin D deficiency has on brain function in health and disease. In addition, results from recent animal studies suggest that vitamin D deficiency during adulthood may exacerbate underlying brain disorders and or worsen recovery from brain stressors. An increasing number of epidemiological studies indicate that vitamin D deficiency is associated with a wide range of neuropsychiatric disorders and neurodegenerative diseases. Vitamin D supplementation is readily available and affordable, and this review highlights the need for further research. Copyright ©2014 by Annual Reviews. All rights reserved.

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