Paul Maruff

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

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Publications (237)769.27 Total impact

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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; · 8.25 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; · 3.58 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. · 3.73 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: 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. 01/2014;
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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
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    ABSTRACT: Associate learning is fundamental to the acquisition of knowledge and plays a critical role in the everyday functioning of the developing child, though the developmental course is still unclear. This study investigated the development of visual associate learning in 125 school age children using the Continuous Paired Associate Learning task. As hypothesized, younger children made more errors than older children across all memory loads and evidenced decreased learning efficiency as memory load increased. Results suggest that age-related differences in performance largely reflect continued development of executive function in the context of relatively developed memory processes.
    PLoS ONE 01/2014; 9(7):e101750. · 3.73 Impact Factor
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    ABSTRACT: High amyloid has been associated with substantial episodic memory decline over 18 and 36 months in healthy older adults and individuals with mild cognitive impairment. However, the nature and magnitude of amyloid-related memory and non-memory change from the preclinical to the clinical stages of Alzheimer's disease has not been evaluated over the same time interval. Healthy older adults (n = 320), individuals with mild cognitive impairment (n = 57) and individuals with Alzheimer's disease (n = 36) enrolled in the Australian Imaging, Biomarkers and Lifestyle study underwent at least one positron emission tomography neuroimaging scan for amyloid. Cognitive assessments were conducted at baseline, and 18- and 36-month follow-up assessments. Compared with amyloid-negative healthy older adults, amyloid-positive healthy older adults, and amyloid-positive individuals with mild cognitive impairment and Alzheimer's disease showed moderate and equivalent decline in verbal and visual episodic memory over 36 months (d's = 0.47-0.51). Relative to amyloid-negative healthy older adults, amyloid-positive healthy older adults showed no decline in non-memory functions, but amyloid-positive individuals with mild cognitive impairment showed additional moderate decline in language, attention and visuospatial function (d's = 0.47-1.12), and amyloid-positive individuals with Alzheimer's disease showed large decline in all aspects of memory and non-memory function (d's = 0.73-2.28). Amyloid negative individuals with mild cognitive impairment did not show any cognitive decline over 36 months. When non-demented individuals (i.e. healthy older adults and adults with mild cognitive impairment) were further dichotomized, high amyloid-positive non-demented individuals showed a greater rate of decline in episodic memory and language when compared with low amyloid positive non-demented individuals. Memory decline does not plateau with increasing disease severity, and decline in non-memory functions increases in amyloid-positive individuals with mild cognitive impairment and Alzheimer's disease. The combined detection of amyloid positivity and objectively-defined decline in memory are reliable indicators of early Alzheimer's disease, and the detection of decline in non-memory functions in amyloid-positive individuals with mild cognitive impairment may assist in determining the level of disease severity in these individuals. Further, these results suggest that grouping amyloid data into at least two categories of abnormality may be useful in determining the disease risk level in non-demented individuals.
    Brain 01/2014; 137(1):221-231. · 9.92 Impact Factor
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    ABSTRACT: Background: We evaluated the utility of longitudinal measures of plasma amyloid-β (Aβ) as a means to identify pre-symptomatic cognitive decline in Alzheimer's disease (AD) when coupled to neuroimaging and neuropsychological parameters. Methods: Participants from the Australian Imaging, Biomarkers and Lifestyle (AIBL) study were grouped based upon cognitive change and changes in measurable levels of neocortical amyloid over 36 months. Participants were classified as those who transitioned for cognitive decline and change in neocortical amyloid, those healthy controls that did not transition, and stable AD participants over 36 months. Results: Comparisons of plasma Aβ levels between the transition and non-transitional groups showed Aβ1-42 and the Aβ1-42/Aβ1-40 ratio were significantly decreased at baseline (p = 0.008 and p = 0.002, respectively) and at 18 months (p = 0.003 and p = 0.004, respectively). Both measures of neocortical amyloid and two previously published composite scores validated the creation of the novel transitional grouping (p < 0.0001). In addition Aβn-42 performed well as a longitudinal prognostic indicator of transition toward cognitive decline, with a significant decrease in the transition group at the 18 month time point (p = 0.01). Conclusion: We demonstrated that baseline plasma Aβ1-42 and the Aβ1-42/Aβ1-40 ratio were putative biomarkers indicative of cognitive decline and validated this result using 18 month data. We created a novel transitional grouping and validated this measure using published measures of neocortical amyloid and composite memory scores. These findings suggest that longitudinal plasma Aβ could contribute to a pre-symptomatic biomarker panel for AD.
    Journal of Alzheimer's disease: JAD 12/2013; · 4.17 Impact Factor
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    ABSTRACT: Biomarkers for Alzheimer disease (AD) can detect the disease pathology in asymptomatic subjects and individuals with mild cognitive impairment (MCI), but their cognitive prognosis remains uncertain. We aimed to determine the prognostic value of β-amyloid imaging, alone and in combination with memory performance, hippocampal atrophy, and apolipoprotein E ε4 status in nondemented, older individuals. A total of 183 healthy individuals (age = 72.0 ± 7.26 years) and 87 participants with MCI (age = 73.7 ± 8.27) in the Australian Imaging, Biomarkers, and Lifestyle study of ageing were studied. Clinical reclassification was performed after 3 years, blind to biomarker findings. β-Amyloid imaging was considered positive if the (11) C-Pittsburgh compound B cortical to reference ratio was ≥1.5. Thirteen percent of healthy persons progressed (15 to MCI, 8 to dementia), and 59% of the MCI cohort progressed to probable AD. Multivariate analysis showed β-amyloid imaging as the single variable most strongly associated with progression. Of combinations, subtle memory impairment (Z score = -0.5 to -1.5) with a positive amyloid scan was most strongly associated with progression in healthy individuals (odds ratio [OR] = 16, 95% confidence interval [CI] = 3.7-68; positive predictive value [PPV] = 50%, 95% CI = 19-81; negative predictive value [NPV] = 94%, 95% CI = 88-98). Almost all amnestic MCI subjects (Z score ≤ -1.5) with a positive amyloid scan developed AD (OR = ∞; PPV = 86%, 95% CI = 72-95; NPV = 100%, 95% CI = 80-100). Hippocampal atrophy and ε4 status did not add further predictive value. Subtle memory impairment with a positive β-amyloid scan identifies healthy individuals at high risk for MCI or AD. Clearly amnestic patients with a positive amyloid scan have prodromal AD and a poor prognosis for dementia within 3 years. Ann Neurol 2013;74:905-913.
    Annals of Neurology 12/2013; 74(6):905-13. · 11.19 Impact Factor
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    ABSTRACT: Brain-derived neurotrophic factor (BDNF) Val66Met polymorphism has previously been implicated in Alzheimer's disease (AD)-related cognitive impairment. We aimed to determine the relationship between BDNF Val66Met and beta-amyloid (Aβ) on cognitive decline, hippocampal atrophy, and Aβ accumulation over 36 months in 165 healthy adults enrolled in the Australian Imaging, Biomarkers and Lifestyle study. In healthy adults with high Aβ, Met carriers showed significant and moderate-to-large declines in episodic memory, executive function, and language, and greater hippocampal atrophy over 36 months, compared with Val/Val homozygotes. BDNF Val66Met was not found to be related to rates of change in cognition or hippocampal volume in healthy adults with low Aβ. BDNF Val66Met did not relate to the amount of Aβ or to the rate of Aβ accumulation in either group. High Aβ levels coupled with Met carriage may be useful prognostic markers of accelerated cognitive decline and hippocampal degeneration in individuals in the preclinical stage of AD.
    Neurobiology of Aging 11/2013; 34(11):2457-64. · 6.17 Impact Factor
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    ABSTRACT: This double-blind study evaluated change in cognitive performance and functional capacity in lurasidone and quetiapine XR-treated schizophrenia patients over a 6-week, placebo-controlled study, followed by a 6-month, double-blind extension. Cognitive performance and functional capacity were assessed with the CogState computerized cognitive battery and the UPSA-B. Analyses were conducted for all subjects, as well as the subsample whose test scores met prespecified validity criteria. No statistically significant differences were found for change in the composite neurocognitive score for lurasidone (80mg/day and 160mg/day) groups, quetiapine XR and placebo in the full sample at week 6. For the evaluable sample (N=267), lurasidone 160mg was superior to both placebo and quetiapine on the neurocognitive composite, while lurasidone 80mg, quetiapine XR, and placebo did not differ. UPSA-B scores were superior to placebo at 6 weeks for all treatments. In the double-blind extension study, analysis of the full sample showed significantly better cognitive performance in the lurasidone (40-160mg) group compared to the quetiapine XR (200-800mg) group at both 3 and 6 months. Cognitive and UPSA-B total scores were significantly correlated at baseline and for change over time. This is the first study to date where the investigational treatment was superior to placebo on both cognitive assessments and a functional coprimary measure at 6 weeks, as well as demonstrated superiority to an active comparator on cognitive assessments at 6 weeks and at 6 months of extension study treatment. These findings require replication, but are not due to practice effects, because of the placebo and active controls.
    European neuropsychopharmacology: the journal of the European College of Neuropsychopharmacology 08/2013; · 3.68 Impact Factor
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    ABSTRACT: ABSTRACT Background: To date evidence of the relationship between cognition and Aβ amyloid during the early stages of Alzheimer's Disease (AD) has been inconsistent. This study aimed to describe the nature and magnitude of the relationship between Aβ amyloid and cognitive performance of individuals without dementia. Methods: Composite cognitive measures were developed from the Australian Imaging Biomarkers and Lifestyle study neuropsychological test battery using data from 768 healthy older adults and 133 adults with mild cognitive impairment (MCI). A subgroup of this sample (174 healthy, 53 MCI) underwent neuroimaging for Aβ amyloid. Results: Within the MCI group individuals with high Aβ amyloid showed selective impairment for memory compared with those with low Aβ amyloid; however, this difference was not evident in the healthy group. Conclusions: The current findings provide further evidence of the relationship between Aβ amyloid and cognition, with memory impairment being the primary symptom of the underlying disease during the prodromal phases of AD.
    International Psychogeriatrics 07/2013; · 2.19 Impact Factor

Publication Stats

4k Citations
769.27 Total Impact Points


  • 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
  • 2005–2012
    • University of Connecticut
      • Department of Psychology
      Storrs, CT, United States
  • 2011
    • Menzies School of Health Research
      Palmerston, Northern Territory, Australia
    • University of Otago
      • Department of Psychological Medicine (Dunedin)
      Dunedin, Otago, New Zealand
    • Melbourne Institute of Technology
      Melbourne, Victoria, Australia
    • St. Vincent Health
      Indianapolis, Indiana, United States
    • Mahidol University
      • Faculty of Medicine Siriraj Hospital
      Bangkok, Bangkok, Thailand
    • The Australian e-Health Research Centre
      Brisbane, Queensland, Australia
  • 2003–2011
    • Saint Vincent Hospital
      Worcester, Massachusetts, United States
  • 2010
    • UNIP Australia Pty Ltd
      Blackburn North, Victoria, Australia
  • 2008–2010
    • Yale University
      • Department of Psychiatry
      New Haven, CT, United States
    • 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
    • University of Waterloo
      • Department of Psychology
      Waterloo, Quebec, Canada
    • Northern Territory Geological Survey
      Palmerston, Northern Territory, Australia
  • 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