Redox Biology and Autism
University of Melbourne, Vic.
“Current treatment options for autism are often associated with limited efficacy and/or significant costs, and lack a pathophysiological basis.”
Kristi-Ann completed her BSc in Psychology at the University of Melbourne in 2007. For her Honours year in 2008, she was based at the Barwon Psychiatric Research Unit and Alcohol and Drug Services at the Geelong Hospital. Her project centred on the prevalence and correlates of psychiatric illness in clients of a methadone maintenance program. She achieved first class honours for her project, and was awarded the Dean’s Award from the Faculty of Science at the University of Melbourne.
In 2009, Kristi-Ann was employed as a Research Assistant with the Department of Paediatrics at the University of Melbourne, where her research focused on positive developmental trajectories in young Australians. During this time, she also completed a Graduate Diploma of Psychology at Deakin University.
Kristi-Ann commenced her PhD in March 2010, under the supervision of Prof Michael Berk, Dr Seetal Dodd and Dr Olivia Dean (all University of Melbourne) and Dr Kylie Gray (Monash University). The aim of her PhD project is to investigate the potential of oxidative pathways as a treatment target in autistic disorder. She selected this project for the exciting opportunity to be involved in a new research area with important implications, and because of her keen interest in autism and awareness of the burden associated with this complex disorder. Treatment and aetiology of autism are currently extremely important research fields and this project may have implications for both.
Current treatment options for autism are often associated with limited efficacy and/or significant costs, and lack a pathophysiological basis. While the aetiology of autism remains poorly understood at present, there is evidence to suggest that oxidative stress may play a role in the pathophysiology of autism. Oxidative stress has long been implicated in neuropsychiatric and neurological disorders and can result either from increased production of reactive species from nitrogen or oxygen, or diminution of oxidative defences. There is an emerging body of literature that demonstrates an abnormality of oxidative homeostasis systemically and centrally in autism, which may be due to an accumulation of free radicals, a depletion of endogenous oxidative defences, or both. In particular, depletion of the primary antioxidant glutathione has been reported in autism, and suggests that an antioxidant treatment strategy targeting the replenishment of glutathione may be a most promising approach.
This study aims to investigate the glutathione precursor, N-acetyl cysteine (NAC) as a treatment for children with autism. The double-blind, randomised trial will be conducted in a total of 80 children, 40 of which will take the NAC treatment and the remaining 40 will take a matched placebo. NAC or placebo will be administered as a single daily 500 mg dose. The study will run over six months after which there will be a 6 month post-baseline follow up to determine the children’s symptoms following the trial. Standard rating scales will be used to assess the children at baseline, 1, 3, 6 and subsequently 12 months. Children will remain on treatment as usual.
This study has the potential to identify a pathophysiologically-based treatment that is non-intrusive, affordable and currently commercially available. If NAC is shown to be effective in improving symptoms of autism, this may have important implications for future treatment and aetiological research.
Supervisors: Professor Michael Berk, Dr Seetal Dodd, Dr Olivia Dean, Dr Kylie Gray & Professor Bruce Tonge