Paul Maruff

University of Melbourne, Melbourne, Victoria, Australia

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Publications (402)2259.62 Total impact

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    ABSTRACT: The stepping-stone variant of the hidden pathway maze learning (HPML) task paradigm has been extensively used to investigate cognitive functions in neuropsychology and neuropharmacology. Previous studies have used total error across trials, as well as rule-break errors and learning errors, to define spatial memory and/or executive function in healthy and impaired adults and children. However, the construct validity of performance measures on HPML tasks has not been established in healthy children. To assess the construct validity of measures of exploratory and rule-break errors on the Groton Maze Learning Task (GMLT) measures of spatial sequence memory (Corsi Blocks Task) and spatial error monitoring (Continuous Paired Associate Learning; CPAL) were used. The results indicate that Corsi span predicted GMLT spatial sequence memory and CPAL accuracy predicted GMLT spatial error monitoring. The construct validity of the GMLT as a measure of spatial memory and executive function are discussed with regard to prior research using HPML tasks in neuropsychological contexts.
    Child Neuropsychology 06/2015; DOI:10.1080/09297049.2015.1038989 · 2.18 Impact Factor
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    ABSTRACT: To better understand the nature and rate of cognitive change across adolescence, the Cogstate Brief Battery (CBB) was utilized to assess psychomotor function, attention, working memory, and visual learning in individuals aged 10 to 18 years old. Since all CBB tasks have equivalent perceptual, motor, and linguistic demands as well as being appropriate for both children and adults, this approach allowed direct across-age comparison of multiple cognitive domains. Exponential decreases in reaction time and linear increases in accuracy were observed across adolescent development in a cross-sectional sample of 38,778 individuals and confirmed in a 5,788 individual longitudinal sample with one-year repeat assessments. These results have important implications for the repeated assessment of cognition during development where expected maturational changes in cognition must be accounted for during cognitive testing.
    Frontiers in Psychology 05/2015; 6. DOI:10.3389/fpsyg.2015.00704 · 2.80 Impact Factor
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    ABSTRACT: This study investigated the prevalence of cognitive impairment in elderly noncardiac surgery patients and any association between preoperative cognitive impairment and postoperative cognitive dysfunction (POCD). Additionally, the incidence of cognitive decline at 12 months after surgery was identified. Three hundred patients for hip joint replacement and 51 nonsurgical controls aged 60 yr or older were studied in a prospective observational clinical trial. All study participants and controls completed a battery of eight neuropsychological tests before surgery and at 7 days, 3 months, and 12 months afterwards. Preoperative cognitive status was assessed using preexisting cognitive impairment (PreCI) defined as a decline of at least 2 SD on two or more of seven neuropsychological tests compared to population norms. POCD and cognitive decline were assessed using the reliable change index utilizing the results of the control group. PreCI was classified in 96 of 300 (32%) patients (95% CI, 23 to 43%). After surgery, 49 of 286 (17%) patients (95% CI, 13 to 22%) and 27 of 284 (10%) patients (95% CI, 6 to 13%) demonstrated POCD at 7 days and 3 months, respectively, while 7 of 271 (3%) patients (95% CI, 1 to 4%) demonstrated cognitive decline at 12 months. Patients with PreCI had a significantly increased incidence of POCD at 7 days and 3 months and cognitive decline at 12 months. Patients with PreCI have an increased incidence of POCD and cognitive decline. PreCI is a good predictor of subsequent POCD and cognitive decline. The incidence of cognitive decline after 12 months in this group of patients is low.
    Anesthesiology 04/2015; DOI:10.1097/ALN.0000000000000671 · 6.17 Impact Factor
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    12th International Conference on Alzheimer's and Parkinson's Disease, Nice, France; 03/2015
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    ABSTRACT: Objective: To explore the subjective experience of memory change in groups at risk of dementia (those with mild cognitive impairment MCI or high β-amyloid (Aβ+) burden) to determine the existence of potential phenomenological typologies. Method: We recruited 123 healthy controls (HC) and individuals with MCI from the Australian Imaging, Biomarker and Lifestyle (AIBL) study. Sixty-7 (HC = 47,MCI = 20) had Aβ scans available for analysis. Semistructured interviews were administered, transcribed, and meaningful phrases extracted from transcripts. Twelve themes were defined and compared across diagnostic status and Aβ status. Results: MCI endorsed more complaints of burdensome coping strategies, increasing frequency, sense of predomination, poor contextualization, progression, dependency, impact on affect, and dismissive attitudes. HCAβ+ acknowledged a progressive memory decline compared to HCAβ-, while MCIAβ+ expressed more burdensome coping strategies, dismissive attitudes, and dependency comparative to either healthy group. Depression was more likely to be related to complaint themes in HCs, while complaint themes were associated with poorer list-learning performance in individuals with MCI. Conclusion: Complaint themes in those with MCI align with the MCI symptom complex, particularly when accompanied with high Aβ load. Healthy Aβ+ individuals acknowledged progressive memory change, suggesting they are aware of memory changes not yet detectable via neuropsychological measures. Depressive symptomatology associated with HC complaints, suggesting certain themes are affect-driven, while complaints in MCI are associated with organically driven functional impairment. Qualitative analysis of SMCs can inform the earliest clinical manifestations of Alzheimer's disease. Our findings can inform diagnostic approaches to the clinical evaluation of memory complaints in the nondemented elderly. (PsycINFO Database Record (c) 2015 APA, all rights reserved).
    Neuropsychology 02/2015; DOI:10.1037/neu0000156 · 3.43 Impact Factor
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    ABSTRACT: AZD6280 is a novel γ-aminobutyric acid A receptor modulator with higher in vitro efficacy at the α2,3 subtypes as compared to the α1 and α5 subtypes. This study compared the pharmacodynamic effects of single oral dose AZD6280 10 mg and 40 mg on the central nervous system with 2 mg of lorazepam. Sixteen healthy males were enrolled into the double-blind, randomized, 4-way crossover study. Two validated central nervous system test batteries, Neurocart and CogState, were administered to measure drug effects on cognition, neurophysiologic function, and psychomotor and subjective feelings. Statistical analysis was performed using mixed model analysis of variance, with fixed factors of treatment, period, time and treatment by time, and random factors of subject, subject by treatment and subject by time, and the average prevalue as covariate. Most pharmacodynamic parameters were affected by lorazepam. AZD6280 induced dose-dependent smaller-than-lorazepam effects on saccadic peak velocity (SPV) (AZD6280, 10 mg vs. AZD6280, 40 mg vs. lorazepam [deg/s]: -22.6 vs. -50.0 vs. -62.9, P < 0.001), whereas the impacts on adaptive-tracking, body-sway, smooth-pursuit, and the one-card-learning tests were significant but much smaller than lorazepam. Thus, the slopes of regression lines for the ΔLog(Sway)-ΔSPV, ΔTracking-ΔSPV, and ΔSmooth-ΔSPV relations were flatter with AZD6280 than with lorazepam. AZD6280 caused a distinct electroencephalography signature from that of lorazepam. The SPV responses to AZD6280 suggest potential concentration-related anxiolytic effects, whereas the smaller SPV-normalized effects of AZD6280 on various non-SPV pharmacodynamic parameters suggest a more favorable side effect profile compared to lorazepam. Overall, the pharmacodynamic profile of AZD6280 matches the pharmacological specificity and selectivity of this compound at the α2,3 γ-aminobutyric acid A receptor subtypes.
    Journal of Clinical Psychopharmacology 02/2015; 35(1):22-33. DOI:10.1097/JCP.0000000000000251 · 3.76 Impact Factor
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    ABSTRACT: Alzheimer disease (AD) is now known to have a long preclinical phase in which pathophysiologic processes develop many years, even decades, before the onset of clinical symptoms. Although the presence of abnormal levels of amyloid-β (Aβ) is associated with higher rates of progression to clinically classified mild cognitive impairment or dementia, little research has evaluated potentially modifiable moderators of Aβ-related cognitive decline, such as anxiety and depressive symptoms. To evaluate the association between Aβ status and cognitive changes, and the role of anxiety and depressive symptoms in moderating Aβ-related cognitive changes in the preclinical phase of AD. In this multicenter, prospective cohort study with baseline and 18-, 36-, and 54-month follow-up assessments, we studied 333 healthy, older adults at hospital-based research clinics. Carbon 11-labeled Pittsburgh Compound B (PiB)-, florbetapir F 18-, or flutemetamol F 18-derived measures of Aβ, Hospital Anxiety and Depression Scale scores, and comprehensive neuropsychological evaluation that yielded measures of global cognition, verbal memory, visual memory, attention, language, executive function, and visuospatial ability. A positive Aβ (Aβ+) status at baseline was associated with a significant decline in global cognition, verbal memory, language, and executive function, and elevated anxiety symptoms moderated these associations. Compared with the Aβ+, low-anxiety group, slopes of cognitive decline were significantly more pronounced in the Aβ+, high-anxiety group, with Cohen d values of 0.78 (95% CI, 0.33-1.23) for global cognition, 0.54 (95% CI, 0.10-0.98) for verbal memory, 0.51 (95% CI, 0.07-0.96) for language, and 0.39 (95% CI, 0.05-0.83) for executive function. These effects were independent of age, educational level, IQ, APOE genotype, subjective memory complaints, vascular risk factors, and depressive symptoms; furthermore, depressive symptoms and subjective memory complaints did not moderate the association between Aβ and cognitive decline. These results provide additional support for the deleterious effect of elevated Aβ levels on cognitive function in preclinical AD. They further suggest that elevated anxiety symptoms moderate the effect of Aβ on cognitive decline in preclinical AD, resulting in more rapid decline in several cognitive domains. Given that there is currently no standard antiamyloid therapy and that anxiety symptoms are amenable to treatment, these findings may help inform risk stratification and management of the preclinical phase of AD.
    JAMA Psychiatry 01/2015; 72(3). DOI:10.1001/jamapsychiatry.2014.2476 · 12.01 Impact Factor
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    ABSTRACT: Memory changes in preclinical Alzheimer's disease (AD) are often characterized by heterogenous trajectories. However, data regarding the nature and determinants of predominant trajectories of memory changes in preclinical AD are lacking. We analyzed data from 333 cognitively healthy older adults who participated in a multicenter prospective cohort study with baseline and 18-, 36-, and 54-month follow-up assessments. Latent growth mixture modeling revealed 3 predominant trajectories of memory change: a below average, subtly declining memory trajectory (30.9%); a below average, rapidly declining memory trajectory (3.6%); and an above average, stable memory trajectory (65.5%). Compared with the stable memory trajectory, high Αβ (relative risk ratio [RRR] = 2.1), and lower Mini-Mental State Examination (RRR = 0.6) and full-scale IQ (RRR = 0.9) scores were independently associated with the subtly declining memory trajectory; and high Αβ (RRR = 8.3), APOE ε4 carriage (RRR = 6.1), and greater subjective memory impairment (RRR = 1.2) were independently associated with the rapidly declining memory trajectory. Compared with the subtly declining memory trajectory group, APOE ε4 carriage (RRR = 8.4), and subjective memory complaints (RRR = 1.2) were associated with a rapidly declining memory trajectory. These results suggest that the preclinical phase of AD may be characterized by 2 predominant trajectories of memory decline that have common (e.g., high Αβ) and unique (e.g., APOE ε4 genotype) determinants. Published by Elsevier Inc.
    Neurobiology of Aging 12/2014; 36(3). DOI:10.1016/j.neurobiolaging.2014.12.015 · 4.85 Impact Factor
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    ABSTRACT: The apolipoprotein E (APOE) ɛ4 allele and high levels of beta-amyloid (Aβ) are associated with episodic memory decline and risk for Alzheimer's disease. However, there is debate about independent or interactive effects of ɛ4 on Aβ-related memory decline in healthy older adults. Healthy older adults with high Aβ burden (n = 84) enrolled in Australian Imaging, Biomarkers, and Lifestyle Study were included in this study. Cognition was measured using the computerized Cogstate Brief Battery at baseline, 18-, 36-, and 54-month follow-ups. Mini Mental State Examination and Clinical Dementia Rating scales were also administered at baseline and each follow-up timepoint. Relative to Aβ+ ɛ4 noncarriers (n = 36), Aβ+ ɛ4 carriers (n = 48) showed significantly faster decline on memory tasks, which was by convention, moderate in magnitude (d = 0.40-0.47). Aβ positivity coupled with APOE ɛ4 was associated with moderately increased decline in memory over a 54-month assessment period, suggesting that, in the preclinical stages of Alzheimer's disease, the manifestation of memory decline in older adults with high Aβ is exacerbated by the presence of APOE ɛ4. Copyright © 2015 Elsevier Inc. All rights reserved.
    Neurobiology of Aging 12/2014; 36(3). DOI:10.1016/j.neurobiolaging.2014.12.008 · 4.85 Impact Factor
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    ABSTRACT: Assessment of risk and early diagnosis of Alzheimer's disease (AD) is a key to its prevention or slowing the progression of the disease. Previous research on risk factors for AD typically utilizes statistical comparison tests or stepwise selection with regression models. Outcomes of these methods tend to emphasize single risk factors rather than a combination of risk factors. However, a combination of factors, rather than any one alone, is likely to affect disease development. Genetic algorithms (GA) can be useful and efficient for searching a combination of variables for the best achievement (eg. accuracy of diagnosis), especially when the search space is large, complex or poorly understood, as in the case in prediction of AD development. Multiple sets of neuropsychological tests were identified by GA to best predict conversions between clinical categories, with a cross validated AUC (area under the ROC curve) of 0.90 for prediction of HC conversion to MCI/AD and 0.86 for MCI conversion to AD within 36 months. This study showed the potential of GA application in the neural science area. It demonstrated that the combination of a small set of variables is superior in performance than the use of all the single significant variables in the model for prediction of progression of disease. Variables more frequently selected by GA might be more important as part of the algorithm for prediction of disease development.
    BMC Bioinformatics 12/2014; 15(Suppl 16):S11. DOI:10.1186/1471-2105-15-S16-S11 · 2.67 Impact Factor
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    ABSTRACT: Physical exercise interventions and cognitive training programs have individually been reported to improve cognition in the healthy elderly population; however, the clinical significance of using a combined approach is currently lacking. This study evaluated whether physical activity (PA), computerized cognitive training and/or a combination of both could improve cognition. In this nonrandomized study, 224 healthy community-dwelling older adults (60-85 years) were assigned to 16 weeks home-based PA (n=64), computerized cognitive stimulation (n=62), a combination of both (combined, n=51) or a control group (n=47). Cognition was assessed using the Rey Auditory Verbal Learning Test, Controlled Oral Word Association Test and the CogState computerized battery at baseline, 8 and 16 weeks post intervention. Physical fitness assessments were performed at all time points. A subset (total n=45) of participants underwent [(18)F] fluorodeoxyglucose positron emission tomography scans at 16 weeks (post-intervention). One hundred and ninety-one participants completed the study and the data of 172 participants were included in the final analysis. Compared with the control group, the combined group showed improved verbal episodic memory and significantly higher brain glucose metabolism in the left sensorimotor cortex after controlling for age, sex, premorbid IQ, apolipoprotein E (APOE) status and history of head injury. The higher cerebral glucose metabolism in this brain region was positively associated with improved verbal memory seen in the combined group only. Our study provides evidence that a specific combination of physical and mental exercises for 16 weeks can improve cognition and increase cerebral glucose metabolism in cognitively intact healthy older adults.
    Translational Research 12/2014; 4(e487). DOI:10.1038/tp.2014.122 · 4.04 Impact Factor
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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; 30(1). DOI:10.1093/arclin/acu068 · 1.92 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; DOI:10.1177/0004867414557161 · 3.77 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 11/2014; 10(6). DOI:10.1016/j.jalz.2013.11.005 · 17.47 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; 65. DOI:10.1016/j.specom.2014.05.002 · 1.55 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; 24(4). DOI:10.1007/s11065-014-9272-7 · 5.40 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; DOI:10.1038/mp.2014.123 · 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. DOI:10.1016/j.jalz.2014.08.103 · 17.47 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; DOI:10.1080/13554794.2014.960429 · 1.38 Impact Factor

Publication Stats

10k Citations
2,259.62 Total Impact Points

Institutions

  • 1998–2015
    • University of Melbourne
      • • Florey Institute of Neuroscience and Mental Health
      • • Department of Psychiatry
      • • Melbourne School of Psychological Sciences
      Melbourne, Victoria, Australia
  • 2014
    • The Florey Institute of Neuroscience and Mental Health
      Melbourne, Victoria, Australia
  • 2012
    • Australian Catholic University
      • Faculty of Arts and Sciences
      Melbourne, Victoria, Australia
  • 1998–2012
    • La Trobe University
      • School of Psychological Science
      Melbourne, Victoria, Australia
  • 2011
    • Melbourne Institute of Technology
      Melbourne, Victoria, Australia
    • Federal University of Minas Gerais
      Cidade de Minas, Minas Gerais, Brazil
    • Menzies School of Health Research
      Palmerston, Northern Territory, Australia
    • The Australian e-Health Research Centre
      Brisbane, Queensland, Australia
    • Mahidol University
      • Faculty of Medicine Siriraj Hospital
      Bangkok, Bangkok, Thailand
  • 2005–2011
    • St. Vincent Hospital
      Green Bay, Wisconsin, United States
    • University of Vic
      • Department of Psychology
      Vic, Catalonia, Spain
  • 2006–2010
    • UNIP Australia Pty Ltd
      Blackburn North, Victoria, Australia
    • St. Vincent Health
      Indianapolis, Indiana, United States
    • University of Connecticut
      • Department of Psychology
      Storrs, Connecticut, United States
  • 2004–2010
    • St. Vincent's Hospital Melbourne
      • Department of Anaesthesia
      Melbourne, Victoria, Australia
  • 2009
    • Massachusetts General Hospital
      Boston, Massachusetts, United States
    • Charles Darwin University
      • Institute of Advanced Studies
      Palmerston, Northern Territory, Australia
    • University of Victoria
      Victoria, British Columbia, Canada
    • Victoria University Melbourne
      Melbourne, Victoria, Australia
  • 2008
    • Queen's University Belfast
      Béal Feirste, Northern Ireland, United Kingdom
  • 2002–2008
    • RMIT University
      • • Department of Psychology
      • • Department of Disability Studies
      Melbourne, Victoria, Australia
  • 2004–2006
    • University of New South Wales
      • St Vincent's Clinical School
      Kensington, New South Wales, Australia
  • 1991–2006
    • Mental Health Research Institute
      Melbourne, Victoria, Australia
  • 1998–2004
    • Swinburne University of Technology
      Melbourne, Victoria, Australia
  • 2003
    • London Research Institute
      Londinium, England, United Kingdom
  • 2001
    • Bendigo Psychology
      Bendigo, Victoria, Australia
  • 2000
    • Universität Heidelberg
      • Department of Geriatric Psychiatry
      Heidelburg, Baden-Württemberg, Germany
  • 1997–1999
    • Royal Melbourne Hospital
      Melbourne, Victoria, Australia