Associate Professor Paul Dawson

Team Leader Developmental Disorders; Head of Education

About me

Associate Professor Paul Dawson is Program Leader of Neurosciences and Cognitive Health, and Team Leader of the Developmental Disorders Group at the Mater Research Institute, University of Queensland. He obtained his PhD in the Department of Medicine at the Princess Alexandra Hospital, and undertook further training at the National Institute of Child Health and Human Development, USA. He has extensive experience with the conduct of clinical genetic screening and biomedical research. He has over 20 years of skills in molecular biology and genetics as an established clinical/biomedical researcher, with a strong interest in the developmental origins of neurodisability. His team is investigating the genetics of intellectual disability, as well as therapeutic approaches for improved neurodevelopmental outcomes in preterm infants. Paul is also an investigator within the Autism Cooperative Research Centre. He contributes to mentoring and teaching of early career staff and students as the Head of Education at Mater Research and as an Associate Professor at the University of Queensland. He is a strong advocate for health and medical research, holding executive positions including the 2012 President of the Australian Society for Medical Research.

Projects

Sulfate levels in preterm babies (SuPreme study)

Each year, 8% of Australian infants are born preterm which places them at increased risk of life-long poor health outcomes, including cerebral palsy and cognitive dysfunction. Our research into the neuroprotective role of sulphate among preterm babies will address this important health issue. The overarching aims of this study are to determine the role of neonatal sulphate status in adverse neurodevelopmental outcomes among preterm-born children and to better understand sulphate biochemistry in order to develop a simple efficacious neuroprotection therapy for preterm infants.

Cell models for investigating autism

Human induced pluripotent stem (iPS) cells are emerging as potential cellular models to recapitulate perturbed steps in neurodevelopment that lead to neuropathy. To date, neurological diseases modelled with iPS cells include schizophrenia, Rett’s syndrome, Huntington’s disease, spinal muscular atrophy and Parkinson’s disease (1). Using established protocols, we will use iPS cells as a cell model of autism.

Investigation of individuals with Idiopathic Intellectual Disability identified within families of normal intellectual capacity and function.

Intellectual Disability affects up to 3% of Australians (over 600,000 individuals) and has a high prevalence in < 15 y.o. children. However, in paediatric and young adult age groups, the majority of Intellectual Disability is not explained by recognised syndromic and/or genetic disorders and therefore may be termed idiopathic. The aetiology of the Intellectual Disability in this group remains unknown and is recognised to be under-researched. Traditional difficulties confronting research into this problem include the likely diverse causative factors; difficulty in phenotyping affected individuals; insufficient resources and lack of sufficiently powerful research methodologies. This study aims to investigate the biological basis of Idiopathic Intellectual Disability.

Investigation of 1) placental biology; 2) fetal development; 3) intellectual disability

Publications

Langford R, Hurrion E, Dawson PA. 2017 Genetics and pathophysiology of sulphate biology. Journal of Genetics and Genome Research. 44(1):7-20.

Dawson PA, Richard K, Perkins A, Zhang Z, Simmons DG. 2017 Review: Nutrient sulfate supply from mother to fetus: placental adaptive responses during human and animal gestation. Placenta. 54:45-51

Dawson PA, Elliott A, Bowling FG. 2017 Sulphate in pregnancy. In, Nutrition in Pregnancy. Ed. J.L. Morrison and T.R.H. Regnault. Vol.2, p.110-123  ISBN 978-3-03842-369-0.

Dawson PA, Petersen S, Rodwell R, Johnson P, Gibbons K, McWhinney A, Bowling FG and McIntyre HD. 2015 Reference intervals for plasma sulfate and urinary sulfate excretion in pregnancy. BMC Pregnancy and Childbirth. 15(1):96.

Dawson PA 2013 Role of sulphate in development. Reproduction. 146(3):R81-89.Dawson PA, Sim P, Mudge D, Cowley D. 2013 Human SLC26A1 gene variants: a pilot study. The Scientific World Journal 2013:541710Simmons DG, Rakoczy J, Jefferis J, Lourie R, McIntyre HD, Dawson PA. 2013 Human placental sulfate transporter mRNA profiling identifies abundant SLC13A4 in syncytiotrophoblasts and SLC26A2 in cytotrophoblasts. 2013 Placenta 34:381-384Jefferis J, Rakoczy J, Simmons DG, Dawson PA 2013 Molecular analysis of the human SLC13A4 sulfate transporter gene promoter. Biochem.Biophys.Res.Comm. 433:79-83Bowling FG, Heussler HS, McWhinney A, Dawson PA 2013 Plasma and urinary sulfate determination in a cohort with autism. Biochem.Genet. 51(1-2):147-153Dawson PA. 2012 The Biological Roles of Steroid Sulfonation: in Steroids (ed.) Intech. Pp http://www.intechopen.com/articles/show/title/the-biological-roles-of-steroid-sulfonationDawson PA 2011 Sulfate in fetal development. Sem.Cell.Devel.Biol. 22(6):652-659.Dawson PA, Russell CS, Lee S, McLeay SC, Gibson SM, Clarke LA, Markovich D 2010 Urolithiasis and hepatotoxicity are linked to the anion transporter Sat1 in mice. J.Clin.Invest 120(3):702-712. 

Research fields

Neonatology; Developmental Biology