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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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Quantitative neurohistological features of frontotemporal degeneration.

TL;DR: FTD is a category of neurodegnerative dementias with varying clinical presentations that is characterized by the progressive degeneration of select populations of cortical neurons, and the molecular neurodegenerative mechanisms that lead to FTD remain to be elucidated.
Journal Article

Molecular markers of primitive neuroectodermal tumors and other pediatric central nervous system tumors. Monoclonal antibodies to neuronal and glial antigens distinguish subsets of primitive neuroectodermal tumors.

TL;DR: It is concluded that PNETs represent a heterogeneous group of pediatric brain tumors capable of neuronal and glial differentiation and can be distinguished from other pediatric central nervous system tumors and to identify subsets of P NETs.
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Multimodal evaluation demonstrates in vivo 18 F-AV-1451 uptake in autopsy-confirmed corticobasal degeneration

TL;DR: F-AV-1451 is a PET radioligand that achieves in vivo binding in Alzheimer’s disease (AD) and autoradiographic evidence of binding to paired helical filaments (PHFs) composed of 3-repeat misfolded tau and 4Rtau characteristic of AD histopathology is reported.
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Brain-Penetrant, Orally Bioavailable Microtubule-Stabilizing Small Molecules Are Potential Candidate Therapeutics for Alzheimer’s Disease and Related Tauopathies

TL;DR: Evaluated compounds from known classes of non-naturally occurring MT-stabilizing small molecules led to the identification of selected triazolopyrimidine and phenylpyrimidines that are orally bioavailable and brain-penetrant without disruption of Pgp function.
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Beta-synuclein modulates alpha-synuclein neurotoxicity by reducing alpha-synuclein protein expression.

TL;DR: In this article, the prion protein promoter alpha-synuclein A53T mouse model of Parkinson's disease was used to study the effect of over-expression of alpha-synuclein in the cortex of transgenic mice.