Paul Maruff

The Florey Institute of Neuroscience and Mental Health, Melbourne, Victoria, Australia

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Publications (248)946.21 Total impact

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    ABSTRACT: We investigated the extent to which decline in memory and working memory in beta-amyloid (Aβ) positive non-demented individuals was related to hippocampal atrophy and Aβ accumulation over 36 months. Cognitively normal older adults (CN) (n = 178) and adults with mild cognitive impairment (MCI) (n = 49) underwent positron emission tomography neuroimaging, magnetic resonance imaging, and cognitive assessments at baseline, 18- and 36-months. Relative to Aβ- CNs, Aβ+ CNs and Aβ+ MCIs showed greater rates of cognitive decline, Aβ accumulation, and hippocampal atrophy. Analysis of interrelationships between these Alzheimer's disease markers in Aβ+ CNs and MCIs indicated that rate of Aβ accumulation was associated with rate of hippocampal atrophy (β = -0.05, p = .037), which was in turn associated independently with rate of decline in memory (β = -0.03, p = .032). This suggests that Aβ accumulation precedes any neurodegeneration or clinical symptoms, and that the relationship between Aβ and cognitive decline is mediated by hippocampal atrophy. © The Author 2014. Published by Oxford University Press. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.
    Archives of Clinical Neuropsychology 12/2014; · 2.00 Impact Factor
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    ABSTRACT: Depression has been shown to be a risk factor for Alzheimer's disease (AD), and in older adults may provide a marker for the beginning of the prodromal phase of AD. The purpose of this systematic review is to examine the relationship between amyloid-β (Aβ), a key biomarker of AD, and depression in older adults. The literature search was limited to studies conducted from 2006 to 2014 that were published in English in peer-reviewed journals. Studies were selected if they included a group of older adults who either met established criteria for Major Depressive Disorder or Dysthymia; or were assessed for depressive symptoms on a standardised measure. Studies were also required to include an outcome variable that was a direct measure of Aβ levels in either blood or cerebrospinal fluid (CSF) samples, or via neuroimaging techniques such as positron emission tomography (PET). Nineteen studies were identified, 15 of which found significant differences in Aβ levels between depressed and non-depressed older adults. However, studies were limited by their cross-sectional design, reliance on blood-based measures of Aβ, and potential sample bias. Future investigations should consider prospective longitudinal design using neuroimaging and CSF measures of Aβ. © The Royal Australian and New Zealand College of Psychiatrists 2014.
    Australian and New Zealand Journal of Psychiatry 11/2014; · 3.77 Impact Factor
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    ABSTRACT: In the control of skeleto-motor movement, it is well established that the less complex, or more automatic a motor task is, the less variability and uncertainty there is in its performance. It was hypothesized that a similar relationship exists for integrated cognitive-motor tasks such as speech where the uncertainty with which actions are initiated may increase when the feedback loop is interrupted or dampened. To investigate this, the Lombard effect was exploited to explore the acoustic impact of background noise on speech during tasks increasing in automaticity. Fifteen healthy adults produced five speech tasks bearing different levels of automaticity (e.g., counting, reading, unprepared monologue) during habitual and altered auditory feedback conditions (Lombard effect). Data suggest that speech tasks relatively free of meaning or phonetic complexity are influenced to a lesser degree by a compromised auditory feedback than more complex paradigms (e.g., contemporaneous speech) on measures of timing. These findings inform understanding of the relative contribution speech task selection plays in measures of speech. Data also aid in understanding the relationship between task automaticity and altered speech production in neurological conditions where dual impairments of movement and cognition are observed (e.g., Huntington’s disease).
    Speech Communication 11/2014; · 1.28 Impact Factor
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    ABSTRACT: Hidden pathway maze learning tasks (HPMLTs) have been used in neuropsychological research and practice for more than 80 years. These tasks require the use of visual and auditory task feedback signals to learn the order and direction of a pathway, typically within a grid of stepping-stones, or alleys. Hidden pathway maze learning tasks are purported to assess both visuospatial learning and executive processes. The original motivation for the HPMLT paradigm for humans was to reduce a complex tactual planning task to one in which decisions could be directly measured by discrete actions at choice points guided by visual cues. Hidden maze learning paradigms were used extensively throughout the 20th century, initially to study exploratory, anticipatory, and goal-related behavior within the context of memory research, and later as an experimental tool in neuropsychology. Computerization of HPMLTs have allowed for the measurement of different move categories according to the rule structure and ipso facto, clinically meaningful differences in memory and monitoring functions during spatial search and learning. Hidden pathway maze learning tests have been used to understand the cognitive effects of ageing, neurological disorders, and psychopharmacological challenges. We provide a review of historical antecedents relevant to contemporary applications of HPMLTs in neuropsychology. It is suggested that contemporary applications of HPMLTs could be advanced by analysis of component operations necessary for efficient performance that can inform theoretical interpretations of this class of tests in clinically meaningful terms.
    Neuropsychology Review 10/2014; · 6.42 Impact Factor
  • 2014 American Academy of Pediatrics National Conference and Exhibition; 10/2014
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    ABSTRACT: Accumulation of β-amyloid (Aβ) in the brain is associated with memory decline in healthy individuals as a prelude to Alzheimer’s disease (AD). Genetic factors may moderate this decline. We examined the role of apolipoprotein E (ε4 carrier[ε4+], ε4 non-carrier[ε4−]) and brain-derived neurotrophic factor (BDNFVal/Val, BDNFMet) in the extent to which they moderate Aβ-related memory decline. Healthy adults (n=333, Mage=70 years) enrolled in the Australian Imaging, Biomarkers and Lifestyle study underwent Aβ neuroimaging. Neuropsychological assessments were conducted at baseline, 18-, 36- and 54-month follow-ups. Aβ positron emission tomography neuroimaging was used to classify participants as Aβ− or Aβ+. Relative to Aβ−ε4−, Aβ+ε4+ individuals showed significantly faster rates of cognitive decline over 54 months across all domains (d=0.40–1.22), while Aβ+ε4− individuals showed significantly faster decline only on verbal episodic memory (EM). There were no differences in rates of cognitive change between Aβ−ε4− and Aβ−ε4+ groups. Among Aβ+ individuals, ε4+/BDNFMet participants showed a significantly faster rate of decline on verbal and visual EM, and language over 54 months compared with ε4−/BDNFVal/Val participants (d=0.90–1.02). At least two genetic loci affect the rate of Aβ-related cognitive decline. Aβ+ε4+/BDNFMet individuals can expect to show clinically significant memory impairment after 3 years, whereas Aβ+ε4+/BDNFVal/Val individuals can expect a similar degree of impairment after 10 years. Little decline over 54 months was observed in the Aβ− and Aβ+ ε4− groups, irrespective of BDNF status. These data raise important prognostic issues in managing preclinical AD, and should be considered in designing secondary preventative clinical trials.
    Molecular Psychiatry 10/2014; · 15.15 Impact Factor
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    ABSTRACT: With increasing numbers of people with Alzheimer's and other dementias across the globe, many countries have developed national plans to deal with the resulting challenges. In the United States, the National Alzheimer's Project Act, signed into law in 2011, required the creation of such a plan with annual updates thereafter. Pursuant to this, the US Department of Health and Human Services (HHS) released the National Plan to Address Alzheimer's Disease in 2012, including an ambitious research goal of preventing and effectively treating Alzheimer's disease by 2025. To guide investments, activities, and the measurement of progress toward achieving this 2025 goal, in its first annual plan update (2013) HHS also incorporated into the plan a set of short, medium and long-term milestones. HHS further committed to updating these milestones on an ongoing basis to account for progress and setbacks, and emerging opportunities and obstacles. To assist HHS as it updates these milestones, the Alzheimer's Association convened a National Plan Milestone Workgroup consisting of scientific experts representing all areas of Alzheimer's and dementia research. The workgroup evaluated each milestone and made recommendations to ensure that they collectively constitute an adequate work plan for reaching the goal of preventing and effectively treating Alzheimer's by 2025. This report presents these Workgroup recommendations.
    Alzheimer's & dementia: the journal of the Alzheimer's Association 10/2014; 10(5 Suppl):S430-52. · 14.48 Impact Factor
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    ABSTRACT: The temporal scale of neuroplasticity following acute alterations in brain structure due to neurosurgical intervention is still under debate. We conducted a longitudinal study with the objective of investigating the postoperative changes in a patient who underwent cerebrovascular surgery and who subsequently lost proprioception in the fingers of her right hand. The results show increased activation in contralesional somatosensory areas, additional recruitment of premotor and posterior parietal areas, and changes in functional connectivity with left postcentral gyrus. These findings demonstrate long-term modifications of cortical organization and as such have important implications for treatment strategies for patients with brain injury.
    Neurocase 09/2014; · 1.05 Impact Factor
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    ABSTRACT: To investigate the association between habitual physical activity levels and brain temporal lobe volumes, and the interaction with the brain-derived neurotrophic factor (BDNF) Val66Met polymorphism.
    Neurology 09/2014; · 8.30 Impact Factor
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    ABSTRACT: Background: The detection of early Alzheimer's disease (AD) can rely on subjective and informant reports of cognitive impairment. However, relationships between subjective cognitive impairment, objectively measured cognitive function, and amyloid-β (Aβ) biomarkers remain unclear. Objective: To determine the extent to which impairment or decline in subjective and informant rated cognitive impairment was associated with memory in healthy older adults with high Aβ. Methods: Healthy older adults (n = 289) enrolled in the Australian Imaging, Biomarkers and Lifestyle (AIBL) study were studied at baseline. Pittsburgh Compound B was used to determine Aβ status at baseline. At baseline and 18 months assessments, subjective memory impairment was assessed using the Memory Complaint Questionnaire and the Short Form of the Informant Questionnaire on Cognitive Decline in the Elderly. Cognition was measured using the Cogstate Brief Battery. Results: At baseline, there were no differences between low and high Aβ groups in subjective or informant-rated cognitive impairment, depressive and anxiety symptoms, or cognitive function. Longitudinal analyses showed moderate decline in learning and working memory over the 18 months in the high Aβ group. However there was no change over time in subjective or informant-rated cognitive impairment, depressive and anxiety symptoms, or cognition in either Aβ group. Conclusions: Although healthy older adults with high Aβ levels show decline in learning and working memory over 18 months, subjective or informant ratings of cognitive impairment do not change over the same period suggesting subjective cognitive impairment may have limited utility for the very early identification of AD.
    Journal of Alzheimer's disease: JAD 08/2014; · 4.17 Impact Factor
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    ABSTRACT: ABSTRACT Background: Autobiographical memory (ABM), personal semantic memory (PSM), and autonoetic consciousness are affected in individuals with mild cognitive impairment (MCI) but their relationship with Alzheimer's disease (AD) biomarkers are unclear. Methods: Forty-five participants (healthy controls (HC) = 31, MCI = 14) completed the Episodic ABM Interview and a battery of memory tests. Thirty-one (HC = 22, MCI = 9) underwent β-amyloid positron emission tomography (PET) and magnetic resonance (MR) imaging. Fourteen participants (HC = 9, MCI = 5) underwent one imaging modality. Results: Unlike PSM, ABM differentiated between diagnostic categories but did not relate to AD biomarkers. Personal semantic memory was related to neocortical β-amyloid burden after adjusting for age and apolipoprotein E (APOE) ɛ4. Autonoetic consciousness was not associated with AD biomarkers, and was not impaired in MCI. Conclusions: Autobiographical memory was impaired in MCI participants but was not related to neocortical amyloid burden, suggesting that personal memory systems are impacted by differing disease mechanisms, rather than being uniformly underpinned by β-amyloid. Episodic and semantic ABM impairment represent an important AD prodrome.
    International psychogeriatrics / IPA. 06/2014;
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    ABSTRACT: Concussion-related cognitive impairments are typically evaluated with repeated neuropsychological assessments where post-injury performances are compared with pre-injury baseline data (baseline method). Many cases of concussions, however, are evaluated in the absence of baseline data by comparing post-injury performances with normative data (normative method). This study aimed to compare the sensitivity and specificity of these two methods using the CogSport/Axon test battery. Normative data and reliable change indices were computed from a non-injured athlete sample (n = 235). Test-retest data from non-injured (n = 260) and recently concussed (n = 29) athlete samples were then used to compare the two methods. The baseline method was found to be more sensitive than the normative method, and both methods had high specificity and overall correct classification rates. This suggests that while the normative method identifies most cases of recent concussions, the baseline method remains a more precise approach to assessing concussion-related cognitive impairments.
    Archives of Clinical Neuropsychology 05/2014; · 2.00 Impact Factor
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    ABSTRACT: AZD7325 is a novel α2,3 -subtype-selective partial GABA-A-receptor modulator. This study investigated the pharmacodynamics of single-oral-dose AZD7325 2mg and 10mgon the central nervous system (CNS) compared to placeboand lorazepam2mg. Thisdouble-blind, randomized, 4-way-crossover studyenrolledsixteen healthymales and administeredtwo validated CNS-test-batteries to measure drug effects on cognitive, neurophysiologic and psychomotor function, and subjective feelings. The pharmacological selectivity of AZD7325 was compared to lorazepamby plotting saccadic peak velocitychange from baseline (ΔSPV) against body sway (ΔSway) and visual analogue scale for alertness(ΔVASalertness ). This analysis has previously been used to identify α2,3 -subtype-selectivity. In contrast with the robust impairment caused by lorazepam (all p<0.05vs. placebo), neither dose of AZD7325 induced statistically significant effects on any pharmacodynamic measurements. Lorazepam-induced SPV-reduction was linearly related to changes in other neurophysiologic biomarkers. In contrast, the slopes of the regression lines were flatter for AZD7325, particularly for the ΔLog(Sway)-ΔSPV relation (estimate slope, AZD7325 10mg vs. lorazepam, difference [95% confidence interval], p-value: -0.00036 vs. -0.00206,0.001704 [0.000639, 0.002768], p=0.0018) and the ΔVASalertness -ΔSPV relationship (0.01855 vs. 0.08216,-0.06360 [-0.1046, -0.02257]; p=0.0024). AZD7325 10 mg and lorazepam induced different response patterns on VAS "feeling high" and electro-encephalography. The characteristic ΔSPV-relative effect profiles of AZD7325 versus lorazepam suggests anxio-selectivity related to α2,3-selective GABAA agonism. However, exploration of higher doses may be warranted. The paucity of effects on most CNS-PD parameters also indicates a mitigated side-effect pattern, with potentially lower cognitive and neurophysiological side-effect burden than non-selective benzodiazepines.
    British Journal of Clinical Pharmacology 05/2014; · 3.69 Impact Factor
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    ABSTRACT: Objective The aim of this study was to examine the effects of testosterone on verbal learning and memory in postmenopausal women.DesignRandomised placebo-controlled trial in which participants were randomized (1:1) to transdermal testosterone gel 300mcg/ day, or identical placebo, for 26 weeks.Patients92 post-menopausal women aged 55-65 years, on no systemic sex hormone therapy.MeasurementsThe primary outcome was the score for the International Shopping List Task (ISLT) of CogState. Secondary outcomes included other CogState domains, the Psychological General Well-Being Index (PGWB) and safety variables.Results89 women, median age 60 years, were included in the primary analysis. Testosterone treatment resulted in statistically significantly better performance for the ISLT (improved verbal learning and memory) compared with placebo, adjusted for age and baseline score (mean difference 1·57; 95%CI 0·13, 3·01) p=0.03). There were no significant differences for other CogState domains or the PGWB scores. At 26 weeks, the median total testosterone was 1·7 nmol/L (interquartile range (IQR) 1·1, 2·4) in the testosterone group and 0·4nmol/L (IQR 0·3, 0·5) in the placebo group.Conclusions The small but statistically significant effect of testosterone treatment on verbal learning and memory in postmenopausal women provides the basis for further clinical trials.This article is protected by copyright. All rights reserved.
    Clinical Endocrinology 04/2014; · 3.40 Impact Factor
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    ABSTRACT: Although beta-amyloid, anxiety and depression have been linked cross-sectionally to reduced memory function in healthy older adults without dementia, prospective data evaluating these associations are lacking. Using data from an observational cohort study of 178 healthy older adults without dementia followed for 3 years, we found that anxiety symptoms significantly moderated the relationship between beta-amyloid level and decline in verbal (Cohen's d = 0.65) and episodic (Cohen's d = 0.38) memory. Anxiety symptoms were additionally linked to greater decline in executive function, irrespective of beta-amyloid and other risk factors. These findings suggest that interventions to mitigate anxiety symptoms may help delay memory decline in otherwise healthy older adults with elevated beta-amyloid.
    The British journal of psychiatry: the journal of mental science 02/2014; · 6.62 Impact Factor
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    ABSTRACT: Background: Autobiographical memory (ABM) refers to the recollection of individual experiences, while personal semantic memory (PSM) refers to personally relevant, but shared, facts. Mild cognitive impairment (MCI) is routinely diagnosed with the aid of neuropsychological tests, which do not tap the ABM and PSM domains. Objective: We aimed to characterize the nature of ABM and PSM retrieval in cognitively healthy (HC) memory complainers, non-memory complainers, and MCI participants, and to investigate the relationship between neuropsychological tests and personal memory. Methods: Gender- and education-matched participants (HC = 80 and MCI = 43) completed the Episodic ABM Interview (EAMI) and a battery of neuropsychological tests. Results: ABM and PSM did not differ between complainers and non-complainers, but were poorer in MCI participants, after accounting for age and depressive symptomatology. There were significant associations between personal memory and objective memory measures were found in MCI participants, but standard cognitive measures were more sensitive to MCI. Conclusion: Personal memorywas compromised in MCI, reflected by lower scores on the EAMI. Memory complaining, assessed by current approaches, did not have an impact on personal memory. Standard subjective questionnaires might not reflect the sorts of concerns that bring individuals to clinical attention. Understanding personal memory function in the elderly may aid in the development of a more sensitive measure of subjective memory concerns.
    Journal of Alzheimer's disease: JAD 02/2014; · 4.17 Impact Factor
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    ABSTRACT: OBJECTIVE: Cross-sectional genetic association studies have reported equivocal results on the relationship between the brain-derived neurotrophic factor (BDNF) Val66Met and risk of Alzheimer's disease (AD). As AD is a neurodegenerative disease, genetic influences may become clearer from prospective study. We aimed to determine whether BDNF Val66Met polymorphism influences changes in memory performance, hippocampal volume, and Aβ accumulation in adults with amnestic mild cognitive impairment (aMCI) and high Aβ. METHODS: Thirty-four adults with aMCI were recruited from the Australian, Imaging, Biomarkers and Lifestyle (AIBL) Study. Participants underwent PiB-PET and structural MRI neuroimaging, neuropsychological assessments and BDNF genotyping at baseline, 18 month, and 36 month assessments. RESULTS: In individuals with aMCI and high Aβ, Met carriers showed significant and large decline in episodic memory (d = 0.90, p = .020) and hippocampal volume (d = 0.98, p = .035). BDNF Val66Met was unrelated to the rate of Aβ accumulation (d = -0.35, p = .401). CONCLUSIONS: Although preliminary due to the small sample size, results of this study suggest that high Aβ levels and Met carriage may be useful prognostic markers of accelerated decline in episodic memory, and reductions in hippocampal volume in individuals in the prodromal or MCI stage of AD.
    PLoS ONE 01/2014; 9(1):e86498. · 3.53 Impact Factor
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    ABSTRACT: Few studies have investigated the effect of an acute psychosocial stress paradigm on impaired attention and working memory in humans. Further, the duration of any stress-related cognitive impairment remains unclear. The aim of this study was to examine the effect of an acute psychosocial stress paradigm, the Trier Social Stress, on cognitive function in healthy volunteers. Twenty-three healthy male and female subjects were exposed to an acute psychosocial stress task. Physiological measures (salivary cortisol, heart rate and blood pressure) and subjective stress ratings were measured at baseline, in anticipation of stress, immediately post-stress and after a period of rest. A neuropsychological test battery including spatial working memory and verbal memory was administered at each time point. Acute psychosocial stress produced significant increases in cardiovascular and subjective measures in the anticipatory and post-stress period, which recovered to baseline after rest. Salivary cortisol steadily declined over the testing period. Acute psychosocial stress impaired delayed verbal recall, attention and spatial working memory. Attention remained impaired, and delayed verbal recall continued to decline after rest. Acute psychosocial stress is associated with an impairment of a broad range of cognitive functions in humans and with prolonged abnormalities in attention and memory. Copyright © 2014 John Wiley & Sons, Ltd.
    Stress and Health 01/2014; · 1.04 Impact Factor
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    ABSTRACT: Background High β-amyloid (Aβ) is associated with faster memory decline in healthy individuals and adults with mild cognitive impairment (MCI). However, longer prospective studies are required to determine if Aβ-related memory decline continues and whether it is associated with increased rate of disease progression. Methods Healthy controls (HCs; n = 177) and adults with MCI (n = 48) underwent neuroimaging for Aβ and cognitive assessment at baseline. Cognition was reassessed 18 and 36 months later. Results Compared with low-Aβ HCs, high-Aβ HC and MCI groups showed moderate decline in episodic and working memory over 36 months. Those with MCI with low Aβ did not show any cognitive decline. Rates of disease progression were increased in the high-Aβ HC and MCI groups. Conclusions In healthy individuals, high Aβ likely indicates that Alzheimer's disease (AD)-related neurodegeneration has begun. Once commenced, the rate of decline in cognitive function remains constant across the preclinical and prodromal stages of AD.
    Alzheimer's & dementia: the journal of the Alzheimer's Association 01/2014; · 14.48 Impact Factor
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    ABSTRACT: Background Abnormal β-amyloid (Aβ) is associated with deleterious changes in central acetylcholinergic tone in the very early stages of Alzheimer's disease (AD), which may be unmasked by a cholinergic antagonist. We aimed to establish an optimal “microdose” of scopolamine for the development of a “cognitive stress test.” Methods Healthy older adults (n = 26, aged 55–75 years) with two risk factors for AD, but with low cortical Aβ burden, completed the Groton Maze Learning Test (GMLT) at baseline and then received scopolamine (0.20 mg subcutaneously). Participants were reassessed at 1, 3, 5, 7, and 8 hours postinjection. Results There were significant differences, of a moderate magnitude, in performance between baseline and 3 hours postinjection for total errors, rule break errors, and the GMLT composite (d ≈ 0.50) that were all unrelated to body mass. Conclusions A very low dose of scopolamine leads to reliable cognitive impairment at 3 hours postdose (Tmax) and full cognitive recovery within 5 hours, supporting its use as a prognostic test paradigm to identify individuals with potential preclinical AD. This paradigm is being implemented in a larger cohort of healthy adults, with high or low Aβ, to identify pharmacodynamic differences between groups.
    Alzheimer's & dementia: the journal of the Alzheimer's Association 01/2014; 10(2):262–267. · 14.48 Impact Factor

Publication Stats

4k Citations
946.21 Total Impact Points

Institutions

  • 2014
    • The Florey Institute of Neuroscience and Mental Health
      Melbourne, Victoria, Australia
  • 2002–2014
    • University of Melbourne
      • • Florey Institute of Neuroscience and Mental Health
      • • Department of Psychiatry
      • • Faculty of Medicine, Dentistry and Health Sciences
      Melbourne, Victoria, Australia
    • Sunshine Hospital
      Bhaganagar, Andhra Pradesh, India
  • 2013
    • Curtin University Australia
      • School of Psychology and Speech Pathology
      Bentley, Western Australia, Australia
  • 2005–2013
    • Charles Darwin University
      • • Institute of Advanced Studies
      • • Menzies School of Health Research
      Palmerston, Northern Territory, Australia
    • University of Vic
      • Department of Psychology
      Vic, Catalonia, Spain
  • 2008–2012
    • Yale University
      • Department of Psychiatry
      New Haven, Connecticut, United States
  • 2005–2012
    • University of Connecticut
      • Department of Psychology
      Storrs, CT, United States
  • 2011
    • Menzies School of Health Research
      Palmerston, Northern Territory, Australia
    • Melbourne Institute of Technology
      Melbourne, Victoria, Australia
    • University of Otago
      • Department of Psychological Medicine (Dunedin)
      Dunedin, Otago, New Zealand
    • The Australian e-Health Research Centre
      Brisbane, Queensland, Australia
    • Mahidol University
      • Faculty of Medicine Siriraj Hospital
      Bangkok, Bangkok, Thailand
    • St. Vincent Health
      Indianapolis, Indiana, United States
  • 2003–2011
    • Saint Vincent Hospital
      Worcester, Massachusetts, United States
  • 2008–2010
    • Alpert Medical School - Brown University
      • Department of Pediatrics
      Providence, Rhode Island, United States
  • 2007–2010
    • St. Vincent's Hospital Melbourne
      • Department of Anaesthesia
      Melbourne, Victoria, Australia
    • Monash University (Australia)
      Melbourne, Victoria, Australia
  • 2009
    • Royal Melbourne Hospital
      Melbourne, Victoria, Australia
  • 2005–2009
    • Victoria University Melbourne
      Melbourne, Victoria, Australia
  • 2002–2009
    • RMIT University
      • Department of Psychology
      Melbourne, Victoria, Australia
  • 1999–2009
    • Swinburne University of Technology
      • Faculty of Life and Social Sciences
      Melbourne, Victoria, Australia
  • 2006
    • University of California, San Diego
      • Department of Psychiatry
      San Diego, CA, United States
  • 2004–2006
    • University of New South Wales
      • St Vincent's Clinical School
      Kensington, New South Wales, Australia
    • Northern Territory Geological Survey
      Palmerston, Northern Territory, Australia
    • University of Waterloo
      • Department of Psychology
      Waterloo, Quebec, Canada
  • 1998–2006
    • La Trobe University
      • • Faculty of Science, Technology and Engineering
      • • School of Psychological Science
      Melbourne, Victoria, Australia
  • 1999–2005
    • Mental Health Research Institute
      Melbourne, Victoria, Australia
  • 2001
    • Westmead Hospital
      Sydney, New South Wales, Australia