Amyloid imaging results from the Australian Imaging, Biomarkers and Lifestyle (AIBL) study of aging.

By C. Rowe, K. Ellis, M. Rimajova, P. Bourgeat, K. Pike, Gareth Jones, J. Fripp, H. Tochon-Danguy, L. Morandeau, G. O'Keefe and 12 more. Neurobiology of Aging, 2010

1,039 citations recorded by the source corpus.

Subfields: Cognitive Neuroscience, Physiology, Psychiatry and Mental health

View Paper: https://www.semanticscholar.org/paper/95adb3d4ce5bbe4e8a6c2c053f47158eced3d6de

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Citations in the corpus

The Centiloid Project: Standardizing Quantitative Amyloid Plaque Estimation by PET (2014, methodology): “…from 34 subjects under the age of 45 (31.5 ± 6.3 years; range 22-43) who were judged to be cognitively normal after a standard neuropsychological and clinical evaluation [7-9] This age range was used because it lends great certainty that the subject will be truly amyloid-negative [10; 11].”
Amyloid Deposition, Hypometabolism, and Longitudinal Cognitive Decline (2012, positive): “Seventy-seven percent of AD patients were florbetapirþ, which is similar to the percentages of AD amyloid positivity reported recently in different populations with florbetapir(24) and PiB,(25) although AD amyloid positivity around 90% or above has also been observed.(22,26,27) This variability coul”
Longitudinal Assessment of Aβ and Cognition in Aging and Alzheimer Disease (2011, background): “participants were subsequently enrolled into the Australian Imaging, Biomarkers, and Lifestyle study of ageing.(19,25) The”
Toward defining the preclinical stages of Alzheimer's disease: Recommendations from the National Institute on Aging-Alzheimer's Association workgroups on diagnostic guidelines for Alzheimer's disease (2011, positive): “…these criteria will enable researchers to characterize further the sequence of biological events over the course of preclinical AD, refine biomarker criteria that will best predict clinical outcome, and ultimately aid in selecting appropriate populations for preclinical therapeutic intervention.”
Brain imaging in Alzheimer disease. (2012, background): “4; Kemppainen et al. 2006; Mintun et al. 2006; Edison et al. 2008; Shin et al. 2008; Hedden et al. 2009; Lowe et al. 2009; Maetzler et al. 2009; Wolk et al. 2009; Devanand et al. 2010; Jagust et al. 2010; Rabinovici et al. 2010; Roe et al. 2010; Rowe et al. 2010; Tolboom et al. 2010).”
The evolution of preclinical Alzheimer’s disease: Implications for prevention trials (2014, positive): “Both the underlying pathophysiological process of AD and its clinical symptomatology represent continua, and the evidence thus far suggests that the pathological and clinical manifestations evolve in parallel, but temporally offset, trajectories (Rowe et al., 2010; Sperling et al., 2011a).”
The amyloid cascade hypothesis for Alzheimer's disease: an appraisal for the development of therapeutics (2011, background): “In the transition from normal cognition to MCI and then to definite AD, although the rate of brain atrophy is accelerated, PIB binding and lowered levels of amyloid-β in the CSF remain abnormal but unchange”
Introduction to Revised Criteria for the Diagnosis of Alzheimer’s Disease: National Institute on Aging and the Alzheimer Association Workgroups (2011, background): “[43] Rowe CC, Ellis KA, Rimajova M, Bourgeat P, Pike KE, Jones G, et al.”
Preclinical Alzheimer’s disease: Definition, natural history, and diagnostic criteria (2016, background): “As a result, it can affect the likelihood of developing AD with age [33,121,122].”
NIA-AA Research Framework: Toward a biological definition of Alzheimer’s disease (2018, neutral): “Abundant human and animal data implicate A and T in the primary pathogenesis of AD [9,100], including the observation that the age-related exponential increase in prevalence of A (by biomarkers and neuropathology) anticipates the age-related exponential increase in prevalence of clinically defined p”