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
An acetylation switch controls TDP-43 function and aggregation propensity
Todd J. Cohen,Andrew W. Hwang,Clark R. Restrepo,Chao-Xing Yuan,John Q. Trojanowski,Virginia M.-Y. Lee +5 more
TL;DR: Evidence that TDP-43 acetylation impairs RNA binding and promotes accumulation of insoluble, hyper-phosphorylated T DP-43 species that largely resemble pathological inclusions in ALS and FTLD-TDP is provided.
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CSF biomarkers in frontotemporal lobar degeneration with known pathology
H. Bian,J. C. van Swieten,Susan Leight,Lauren Massimo,Elisabeth M. Wood,Mark S. Forman,Peachie Moore,I. de Koning,Christopher M. Clark,Sonia M. Rosso,John Q. Trojanowski,Virginia M.-Y. Lee,Murray Grossman +12 more
TL;DR: The ratio of CSF tau/Aβ42 is a sensitive and specific biomarker at discriminating frontotemporal lobar degeneration from Alzheimer disease in patients with known pathology.
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TrkC expression predicts good clinical outcome in primitive neuroectodermal brain tumors
Michael A. Grotzer,Anna J. Janss,Kar-Ming Fung,Jaclyn A. Biegel,Leslie N. Sutton,Lucy B. Rorke,Huaqing Zhao,Avital Cnaan,Peter C. Phillips,Virginia M.-Y. Lee,John Q. Trojanowski +10 more
TL;DR: Assessment of TrkC mRNA levels may aid in treatment planning for patients with PNETs and should be incorporated prospectively into PNET clinical trials.
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Frontotemporal lobar degeneration: defining phenotypic diversity through personalized medicine
David J. Irwin,Nigel J. Cairns,Murray Grossman,Corey T. McMillan,Edward B. Lee,Vivianna M. Van Deerlin,Virginia M.-Y. Lee,John Q. Trojanowski +7 more
TL;DR: It is proposed that combining several of these biomarker modalities will improve diagnostic specificity in FTLD through a personalized medicine approach and enhance power for clinical trials focused on slowing or preventing progression of spread of tau, TDP-43 and other FTLD-associated pathologies.
Journal ArticleDOI
Evidence for Ordering of Alzheimer Disease Biomarkers
Clifford R. Jack,Prashanthi Vemuri,Heather J. Wiste,Stephen D. Weigand,Paul S. Aisen,John Q. Trojanowski,Leslie M. Shaw,Matt A. Bernstein,Ronald C. Petersen,Michael W. Weiner,David S. Knopman +10 more
TL;DR: A reduction in the CSF Aβ42 level denotes a pathophysiological process that significantly departs from normality (ie, becomes dynamic) early, whereas theCSF total tau level and the adjusted hippocampal volume are biomarkers of downstream pathophysiology processes.