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Chester A. Mathis
Researcher at University of Pittsburgh
Publications - 318
Citations - 40245
Chester A. Mathis is an academic researcher from University of Pittsburgh. The author has contributed to research in topics: Pittsburgh compound B & Alzheimer's disease. The author has an hindex of 90, co-authored 311 publications receiving 37052 citations. Previous affiliations of Chester A. Mathis include University of California, Berkeley.
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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
TL;DR: The results suggest that PET imaging with the novel tracer, PIB, can provide quantitative information on amyloid deposits in living subjects.
Journal ArticleDOI
Molecular, Structural, and Functional Characterization of Alzheimer's Disease: Evidence for a Relationship between Default Activity, Amyloid, and Memory
Randy L. Buckner,Abraham Z. Snyder,Benjamin J. Shannon,Gina N. LaRossa,Rimmon Sachs,Anthony F. Fotenos,Yvette I. Sheline,William E. Klunk,Chester A. Mathis,John C. Morris,Mark A. Mintun +10 more
TL;DR: One possibility is that lifetime cerebral metabolism associated with regionally specific default activity predisposes cortical regions to AD-related changes, including amyloid deposition, metabolic disruption, and atrophy, which may be part of a network with the medial temporal lobe whose disruption contributes to memory impairment.
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Inverse relation between in vivo amyloid imaging load and cerebrospinal fluid Abeta42 in humans.
Anne M. Fagan,Mark A. Mintun,Robert H. Mach,Sang-Yoon Lee,Carmen S. Dence,Aarti R. Shah,Gina N. LaRossa,Michael L. Spinner,William E. Klunk,Chester A. Mathis,Steven T. DeKosky,John C. Morris,David M. Holtzman +12 more
TL;DR: Amyloid‐β42 (Aβ42) appears central to Alzheimer's disease pathogenesis and is a major component of amyloid plaques, and its decrease may reflect plaques acting as an Aβ42 “sink,” hindering transport of soluble A β42 between brain and CSF.
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[11C]PIB in a nondemented population: potential antecedent marker of Alzheimer disease.
Mark A. Mintun,Gina N. LaRossa,Yvette I. Sheline,Carmen S. Dence,S. Y. Lee,Robert H. Mach,William E. Klunk,Chester A. Mathis,Steven T. DeKosky,John C. Morris +9 more
TL;DR: Elevated [11C]PIB binding in nondemented subjects suggests that [11 C]P IB amyloid imaging may be sensitive for detection of a preclinical Alzheimer disease state.
Journal ArticleDOI
Synthesis and evaluation of 11c-labeled 6-substituted 2-arylbenzothiazoles as amyloid imaging agents
Chester A. Mathis,Yanming Wang,Daniel P. Holt,Guo Feng Huang,Manik L. Debnath,William E. Klunk +5 more
TL;DR: In vitro and in vivo properties of [(11)C]6-OH-BTA-1 support the choice of this derivative for further evaluation in human subject studies of brain Abeta deposition, and indicate the selective binding of the compound to amyloid plaques and cerebrovascular amyloids.