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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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Book ChapterDOI

Purification of paired helical filament tau and normal tau from human brain tissue.

TL;DR: This chapter describes a procedure to effectively purify PHF–tau and soluble normal tau preparations from human brain.
Journal ArticleDOI

Motor neuron disease clinically limited to the lower motor neuron is a diffuse TDP-43 proteinopathy.

TL;DR: The next revision of the El Escorial criteria for the diagnosis of ALS should include MND patients with disease clinically limited to the LMN and PMA as variants of ALS, which like classical ALS, are TDP-43 proteinopathies.
Journal ArticleDOI

Animal models of medulloblastomas and related primitive neuroectodermal tumors. A review.

TL;DR: This review summarizes current understanding of the cell biology of human PNET, particularly medulloblastomas, and it highlights the most salient features of representative in vivo model systems ofhuman PNET that are relevant to future studies of these tumors.
Journal ArticleDOI

An extensive network of PHFτ-rich dystrophic neurites permeates neocortex and nearly all neuritic and diffuse amyloid plaques in Alzheimer disease

TL;DR: Re‐examination of amyloid deposits with antibodies to Aβ and PHFτ by conventional and confocal microscopy using double label immunohistochemistry showed that PHF τ is a component of both diffuse and neuritic plaques in AD.
Journal ArticleDOI

A68 is a component of paired helical filaments of Gerstmann-Sträussler-Scheinker disease, Indiana kindred

TL;DR: The results indicate that A68 is a component of NFT in this family as it is in Alzheimer's disease, and suggest that post-translational modifications of tau leading to formation of A68 are not unique to Alzheimer’s disease.