J
John Q. Trojanowski
Researcher at University of Pennsylvania
Publications - 1538
Citations - 245534
John Q. Trojanowski is an academic researcher from University of Pennsylvania. The author has contributed to research in topics: Dementia & Alzheimer's disease. The author has an hindex of 226, co-authored 1467 publications receiving 213948 citations. Previous affiliations of John Q. Trojanowski include Vanderbilt University & University of California, San Francisco.
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Journal ArticleDOI
Association of plasma and cortical amyloid beta is modulated by APOE ε4 status.
Shanker Swaminathan,Shannon L. Risacher,Karmen K. Yoder,John D. West,Li Shen,Sungeun Kim,Mark Inlow,Mark Inlow,Tatiana Foroud,William J. Jagust,Robert A. Koeppe,Chester A. Mathis,Leslie M. Shaw,John Q. Trojanowski,Holly Soares,Paul S. Aisen,Ronald C. Petersen,Michael W. Weiner,Andrew J. Saykin +18 more
TL;DR: Apolipoprotein E (APOE) ε4 allele's role as a modulator of the relationship between soluble plasma amyloid beta (Aβ) and fibrillar brain Aβ measured by Pittsburgh compound B positron emission tomography ([11C]PiB PET) has not been assessed.
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High-throughput quantitative histological analysis of Alzheimer's disease pathology using a confocal digital microscanner
TL;DR: The microscanner may be generally applicable to a wide variety of human histopathologies and their animal models, wherever rapid unbiased quantitative analysis is needed, and quantifies structures labeled with fluorescent or nonfluorescent probes.
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Biomarkers in frontotemporal lobar degenerations--progress and challenges.
TL;DR: Progress has been made in FTLD biomarkers, including clinical phenotype/feature characterization, neuropsychological analysis, CSF and plasma analytes, and patterns of brain atrophy and network dysfunction detectable on brain imaging, but there remains no reliable biomarker for early detection of FTLD or prediction of underlying FTLD pathologic change.
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Neurofilament reassembly in vitro: biochemical, morphological and immuno-electron microscopic studies employing monoclonal antibodies to defined epitopes.
TL;DR: It is concluded that purified mammalian axonal NF triplet proteins, independent of their phosphorylation state, rapidly and efficiently reassemble in vitro to generate characteristic 10-nm filaments.
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The transcriptional activation domain of VP16 is required for efficient infection and establishment of latency by HSV-1 in the murine peripheral and central nervous systems.
Ruth Tal-Singer,Rath Pichyangkura,Eugene Chung,Todd M. Lasner,Todd M. Lasner,Bruce Randazzo,Bruce Randazzo,John Q. Trojanowski,Nigel W. Fraser,Nigel W. Fraser,Steven J. Triezenberg +10 more
TL;DR: A deletion mutant completely lacking the activation domain of VP16 (RP5) was unable to replicate to any detectable level or to efficiently establish latent infections in the peripheral and central nervous systems of immunocompetent mice, where RP5 is severely neuroattenuated in the murine model of HSV infection.