Cardiff University is a research university located in the Cathays Park area of Cardiff, Wales, United Kingdom. It received its Royal charter in 1883 and is a member of the Russell Group of Universities. The university is consistently recognised as providing high quality research-based university education in Wales. Wikipedia.
Owen M.J.,University of Cardiff
Neuron | Year: 2014
Recent findings in psychiatric genetics have crystallized concerns that diagnostic categories used in the clinic map poorly onto the underlying biology. If we are to harness developments in genetics and neuroscience to understand disease mechanisms and develop new treatments, we need new approaches to patient stratification that recognize the complexity and continuous nature of psychiatric traits and that are not constrained by current categorical approaches. Recognizing this, the National Institute for Mental Health (NIMH) has developed a novel framework to encourage more research of this kind. The implications of these recent findings and funding policy developments for neuroscience research are considerable. © 2014 Elsevier Inc.
Owen M.J.,University of Cardiff
Schizophrenia Bulletin | Year: 2012
From the perspective of those of us working on the genetics of schizophrenia, recent progress in identifying specific genetic risk factors at highly robust levels of statistical significance has been striking. However, the prevailing response among other schizophrenia researchers and some funders, families, and sufferers is often one of disappointment. In particular, it is often claimed that these discoveries explain only a small proportion of the genetic risk and hence tell us little about the nature of schizophrenia. The purpose of this article is to persuade you that recent genetic findings, while only revealing the tip of a complex genetic iceberg, already have profound implications for our general understanding of the classification and pathogenesis of schizophrenia and related disorders and that these have implications for schizophrenia research of all kinds. © 2012 The Author.
Collishaw S.,University of Cardiff
Journal of Child Psychology and Psychiatry and Allied Disciplines | Year: 2015
Background: Child and adolescent mental health problems are common, associated with wide-ranging functional impairments, and show substantial continuities into adult life. It is therefore important to understand the extent to which the prevalence of mental health problems has changed over time, and to identify reasons behind any trends in mental health. Scope and Methodology: This review evaluates evidence on whether the population prevalence of child and adolescent mental health problems has changed. The primary focus of the review is on epidemiological cross-cohort comparisons identified by a systematic search of the literature (using the Web of Knowledge database). Findings: Clinical diagnosis and treatment of child and adolescent psychiatric disorders increased over recent decades. Epidemiological comparisons of unselected population cohorts using equivalent assessments of mental health have found little evidence of an increased rate of ADHD, but cross-cohort comparisons of rates of ASD are lacking at this time. Findings do suggest substantial secular change in emotional problems and antisocial behaviour in high-income countries, including periods of increase and decrease in symptom prevalence. Evidence from low- and middle-income countries is very limited. Possible explanations for trends in child and adolescent mental health are discussed. The review also addresses how cross-cohort comparisons can provide valuable complementary information on the aetiology of mental illness. © 2014 Association for Child and Adolescent Mental Health.
Morgan B.P.,University of Cardiff
Acta neuropathologica communications | Year: 2014
INTRODUCTION: Inflammation and complement activation are firmly implicated in the pathology of multiple sclerosis; however, the extent and nature of their involvement in specific pathological processes such as axonal damage, myelin loss and disease progression remains uncertain. This study aims to bring clarity to these questions.RESULTS: We describe a detailed immunohistochemical study to localise a strategically selected set of complement proteins, activation products and regulators in brain and spinal cord tissue of 17 patients with progressive multiple sclerosis and 16 control donors, including 9 with central nervous system disease. Active, chronic active and chronic inactive multiple sclerosis plaques (35 in total) and non-plaque areas were examined.Multiple sclerosis plaques were consistently positive for complement proteins (C3, factor B, C1q), activation products (C3b, iC3b, C4d, terminal complement complex) and regulators (factor H, C1-inhibitor, clusterin), suggesting continuing local complement synthesis, activation and regulation despite the absence of other evidence of ongoing inflammation. Complement staining was most apparent in plaque and peri-plaque but also present in normal appearing white matter and cortical areas to a greater extent than in control tissue. C1q staining was present in all plaques suggesting a dominant role for the classical pathway. Cellular staining for complement components was largely restricted to reactive astrocytes, often adjacent to clusters of microglia in close apposition to complement opsonised myelin and damaged axons.CONCLUSIONS: The findings demonstrate the ubiquity of complement involvement in multiple sclerosis, suggest a pathogenic role for complement contributing to cell, axon and myelin damage and make the case for targeting complement for multiple sclerosis monitoring and therapy.
Craddock N.,University of Cardiff |
Sklar P.,Mount Sinai School of Medicine
The Lancet | Year: 2013
Studies of families and twins show the importance of genetic factors affecting susceptibility to bipolar disorder and suggest substantial genetic and phenotypic complexity. Robust and replicable genome-wide significant associations have recently been reported in genome-wide association studies at several common polymorphisms, including variants within the genes CACNA1C, ODZ4, and NCAN. Strong evidence exists for a polygenic contribution to risk (ie, many risk alleles of small effect). A notable finding is the overlap of susceptibility between bipolar disorder and schizophrenia for several individual risk alleles and for the polygenic risk. By contrast, genomic structural variation seems to play a smaller part in bipolar disorder than it does in schizophrenia. Together, these genetic findings suggest directions for future studies to delineate the aetiology and pathogenesis of bipolar disorder, indicate the need to re-evaluate our diagnostic classifications, and might eventually pave the way for major improvements in clinical management. © 2013 Elsevier Ltd.