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
A frontal variant of Alzheimer's disease exhibits decreased calcium-independent phospholipase A2 activity in the prefrontal cortex.
Konrad Talbot,Robert A. Young,Camille Jolly-Tornetta,Virginia M.-Y. Lee,John Q. Trojanowski,Bryan A. Wolf +5 more
TL;DR: Low levels of Ca(2+)-independent PLA2 activity in frontal AD may reflect a compensatory response to pathologically accelerated phospholipid metabolism early in the disorder, which could cause an early elevation of prefrontal free fatty acids.
Journal ArticleDOI
Selective degeneration fo Purkinje cells with Lewy body-like inclusions in aged NFHLACZ transgenic mice.
Pang-Hsien Tu,K. A. Robinson,F. De Snoo,J. Eyer,Alan Peterson,Virginia M.-Y. Lee,John Q. Trojanowski +6 more
TL;DR: The sequestration of cellular organelles in type II inclusions may isolate and impair the function of these organlles, thereby rendering Purkinje cells selectively vulnerable to degeneration with age as in neurodegenerative diseases of the elderly characterized by accumulation of LBs.
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TDP-43 Promotes Neurodegeneration by Impairing Chromatin Remodeling
Amit Berson,Ashley Sartoris,Raffaella Nativio,Vivianna M. Van Deerlin,Jon B. Toledo,Sílvia Porta,Shichong Liu,Chia Yu Chung,Benjamin A. Garcia,Virginia M.-Y. Lee,John Q. Trojanowski,F. Brad Johnson,Shelley L. Berger,Nancy M. Bonini +13 more
TL;DR: It is found that TDP-43-mediated neurodegeneration causes impaired chromatin dynamics that prevents appropriate expression of protective genes through compromised function of the chromatin remodeler Chd1/CHD2.
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Intraneuronal and extracellular neurofibrillary tangles exhibit mutually exclusive cytoskeletal antigens.
TL;DR: Observations indicate that neurofilament‐like and tau‐like epitopes can be lost from NFTs in situ, and that at least two populations of morphologically and immunochemically distinct N FTs exist.
Journal Article
Chemical and immunological heterogeneity of fibrillar amyloid in plaques of Alzheimer's disease and Down's syndrome brains revealed by confocal microscopy.
TL;DR: It is suggested that anti-A beta antibodies and thioS stain similar; as well as different forms of fibrillar amyloid, which may be important for the pathogenesis of AD and elderly Down's syndrome patients.