Journal ArticleDOI
Imaging brain amyloid in Alzheimer's disease with Pittsburgh Compound-B.
William E. Klunk,Henry Engler,Agneta Nordberg,Yanming Wang,G. Blomqvist,Daniel P. Holt,Mats Bergström,Irina Savitcheva,Guo Feng Huang,Sergio Estrada,Birgitta Ausén,Manik L. Debnath,Julien Barletta,Julie C. Price,Johan Sandell,Brian J. Lopresti,Anders Wall,Pernilla Koivisto,Gunnar Antoni,Chester A. Mathis,Bengt Långström +20 more
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TLDR
The results suggest that PET imaging with the novel tracer, PIB, can provide quantitative information on amyloid deposits in living subjects.Abstract:
This report describes the first human study of a novel amyloid-imaging positron emission tomography (PET) tracer, termed Pittsburgh Compound-B (PIB), in 16 patients with diagnosed mild AD and 9 controls. Compared with controls, AD patients typically showed marked retention of PIB in areas of association cortex known to contain large amounts of amyloid deposits in AD. In the AD patient group, PIB retention was increased most prominently in frontal cortex (1.94-fold, p = 0.0001). Large increases also were observed in parietal (1.71-fold, p = 0.0002), temporal (1.52-fold, p = 0.002), and occipital (1.54-fold, p = 0.002) cortex and the striatum (1.76-fold, p = 0.0001). PIB retention was equivalent in AD patients and controls in areas known to be relatively unaffected by amyloid deposition (such as subcortical white matter, pons, and cerebellum). Studies in three young (21 years) and six older healthy controls (69.5 +/- 11 years) showed low PIB retention in cortical areas and no significant group differences between young and older controls. In cortical areas, PIB retention correlated inversely with cerebral glucose metabolism determined with 18F-fluorodeoxyglucose. This relationship was most robust in the parietal cortex (r = -0.72; p = 0.0001). The results suggest that PET imaging with the novel tracer, PIB, can provide quantitative information on amyloid deposits in living subjects.read more
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11C PiB and structural MRI provide complementary information in imaging of Alzheimer's disease and amnestic mild cognitive impairment.
Clifford R. Jack,Val J. Lowe,Matthew L. Senjem,Stephen D. Weigand,Bradley J. Kemp,Maria M. Shiung,David S. Knopman,Bradley F. Boeve,William E. Klunk,Chester A. Mathis,Ronald C. Petersen +10 more
TL;DR: Comparisons of cognitive performance and diagnostic group-wise discrimination between cognitively normal, amnestic mild cognitive impairment (MCI) and Alzheimer's disease subjects with MRI-based measures of hippocampal volume and PiB retention and the topographic distribution of amyloid deposition and grey matter loss were compared.
Journal ArticleDOI
Cerebrospinal Fluid tau/β-Amyloid42 Ratio as a Prediction of Cognitive Decline in Nondemented Older Adults
Anne M. Fagan,Catherine M. Roe,Chengjie Xiong,Mark A. Mintun,John C. Morris,David M. Holtzman +5 more
TL;DR: The very mildest symptomatic stage of AD exhibits the same CSF biomarker phenotype as more advanced AD, and CSF tau/Abeta(42) ratios show strong promise as antecedent (preclinical) biomarkers that predict future dementia in cognitively normal older adults.
Journal ArticleDOI
Islet Amyloid Polypeptide, Islet Amyloid, and Diabetes Mellitus
TL;DR: This review deals both with physiological aspects of IAPP and with the pathophysiological role of aggregated forms of I APP, including mechanisms whereby human IAPP forms toxic aggregates and amyloid fibrils.
Journal ArticleDOI
The Cortical Signature of Alzheimer's Disease: Regionally Specific Cortical Thinning Relates to Symptom Severity in Very Mild to Mild AD Dementia and is Detectable in Asymptomatic Amyloid-Positive Individuals
Bradford C. Dickerson,Akram Bakkour,David H. Salat,Eric Feczko,Jenni Pacheco,Douglas N. Greve,Fran Grodstein,Christopher I. Wright,Christopher I. Wright,Deborah Blacker,H. Diana Rosas,Reisa A. Sperling,Alireza Atri,John H. Growdon,Bradley T. Hyman,John C. Morris,Bruce Fischl,Bruce Fischl,Randy L. Buckner,Randy L. Buckner +19 more
TL;DR: In this paper, an exploratory map of cortical thinning in mild Alzheimer's disease was used to define regions of interest that were applied in a hypothesis-driven fashion to other subject samples.
Journal ArticleDOI
The scientific and clinical basis for the treatment of Parkinson disease (2009)
TL;DR: This monograph provides an overview of the management of PD patients, with an emphasis on pathophysiology, and the results of recent clinical trials to provide physicians with an understanding of the different treatment options that are available for managing the different stages of the disease and the scientific rationale of theDifferent approaches.
References
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Graphical Evaluation of Blood-to-Brain Transfer Constants from Multiple-Time Uptake Data. Generalizations:
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