Dr Naomi Wray

Queensland Institute of Medical Research
Mental Health Pilot Study 2010

Naomi Wray is an ARC Future Fellow and an NHMRC Honorary Senior Research Fellow. She is a statistical geneticist and leads the Psychiatric Genetics Laboratory at the Queensland Institute of Medical Research. Her early training was in quantitative genetics with application in livestock which provides a strong theoretical foundation for her research today. She moved to Australia to join QIMR in 2005.

She is currently involved in a number of international collaborations of genome-wide association studies (GWAS) for psychiatric disorders, including the International Schizophrenia Consortium, the Psychiatric GWAS Consortium for major depression and the Anxiety Genetics Study Team. Her current research also focuses on prediction of genetic risk to disease from genome-wide association data.
 
Key publications 2009-2010:
1.       Wray NR, Visscher PM (2010) Narrowing the boundaries of the genetic architecture of schizophrenia. Schizophrenia Bulletin 36:14-23
2.       Wray NR, James MR, Gordon SD, Dumenil T, Ryan L, Coventry WL, Statham DJ, PergadiaML, MaddenPAF, HeathAC, MontgomeryGW, Martin.Accurate, large-scale genotyping of 5HTTLPR and flanking SNPs in an association study of depression, anxiety and personality measures. Biological Psychiatry 66: 468-476   
3.       Evans DM, Visscher PM, Wray NR. Harnessing the Information Contained Within Genome-wide Association Studies to Improve Individual Prediction of Complex Disease Risk. Human Molecular Genetics 18: 3525-3531 
4.       Purcell SM, Wray NR, Stone JL, Visscher PM, O’Donovan MC, Sullivan PF, Sklar P, International Schizophrenia Consortium (2009) Common polygenic variation plays an important role in schizophrenia. Nature 460: 748-752   

SUMMARY OF PROJECT:
Genetic variation of pro-inflammatory markers and their association with depression in adolescence
 
The need
The 2007 Australian National Survey of Mental Health and Wellbeing of 16-85 year-olds in Australia showed that in any year 4% of Australians suffer a depressive episode, with lifetime risk of 12%. Depressive syndromes in adolescents are particularly serious because they carry a considerable risk for recurrence throughout adult lifeand subsequent psychosocial impairment. The genetic contribution to variation in liability to early age of onset depression is high.
 
The theory
Typical symptoms of infection are tiredness, fragmented sleep, irritable, loss of interest in food and surroundings, mild cognitive difficulties such as impaired attention. Sickness is a normal response to infection, yet the symptoms mimic the symptoms of clinical depression. The sickness response is characterized by complex changes in the endocrine system mediated by pro-inflammatory cytokines. In fact, cytokines act as neuromodulators in the absence of an immune challenge, generating a hypothesis that they have a role in causative role in the etiology of major depression.
 
The theory of cytokine induced depression is compelling, is supported by evidence from a range of studies and complements rather than replaces other theories of depression. However, the published studies are, on the whole, small scale and only one small study has focussed on adolescents. A more comprehensive study on larger samples, with a range of complementary measures is needed to fully understand the relationship between cytokines and depression and particularly whether cytokines contribute to the causes of depressive symptoms in adolescence.
 
The study
Our aim is to investigate the relationship between circulating levels of cytokines and measures of depression in a large community sample of adolescent twins and their siblings. The family design ensures that this study sample is genetically informative. The sample has been measured at ages 12, 14 and 16 years using a comprehensive battery of psychiatric and personality questionnaires and cognitive tests. The study sample is being followed-up into early adulthood. At each age, blood has been collected and a battery of biochemical markers has been measured. Genome-wide genotypes are available for the entire cohort including parents. Measurement of cytokine levels in this phenotypically and genetically rich resource will provide a powerful handle for investigating whether genetic variation in levels of cytokines is associated with genetic variation in depression, personality and cognition.