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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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Vertical gaze ophthalmoplegia: selective paralysis of downgaze.

John Q. Trojanowski, +1 more
- 01 Jun 1980 - 
TL;DR: A 58-year-old man developed a selective supranuclear paralysis of downgaze, which was repeatedly documented until it completely resolved after 6 weeks, with a bilaterally symmetric old infarct in the mesodiencephalic region.
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Plasma biomarkers of depressive symptoms in older adults

TL;DR: An unbiased analysis of 146 plasma analytes in a multiplex biochemical biomarker study in relation to number of depressive symptoms endorsed by 566 participants in the Alzheimer's Disease Neuroimaging Initiative (ADNI) found Analytes that were most highly associated with depressive symptoms included hepatocyte growth factor, insulin polypeptides, pregnancy-associated plasma protein-A and vascular endothelial growth factor.
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Monoclonal antibodies to purified cortical Lewy bodies recognize the mid-size neurofilament subunit.

TL;DR: Results support the hypothesis that NF subunits are integral components of LBs and lead to novel strategies for the antemortem diagnosis of LB disorders as well as to insight into the role LBs play in the degeneration of affected neurons in these disorders.
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Spinal Cord Neurofibrillary Pathology in Alzheimer Disease and Guam Parkinsonism-Dementia Complex

TL;DR: The immunohistochemical profile of these NFTs indicates that they are composed of hyperphosphorylated tau protein like their counterparts in the brains of neurodegenerative disease patients and controls and exhibited the presence of all 6 tau isoforms similar to that from AD and ALS/PDC cortical gray matter.
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Accumulation of Intracellular Amyloid-β Peptide (Aβ 1–40) in Mucopolysaccharidosis Brains

TL;DR: At least some of the metabolic defects that lead to accumulations of glycosaminoglycans in MPS also are associated with an increase in immunoreactive A beta within the cytoplasmic compartment where they could contribute to the dysfunction and death of affected cells in these disorders, but not induce the formation of plaques and tangles.