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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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Evaluation of the brain-penetrant microtubule-stabilizing agent, dictyostatin, in the PS19 tau transgenic mouse model of tauopathy

TL;DR: The efficacy of another small molecule brain-penetrant MT-stabilizing agent, dictyostatin, is demonstrated in the PS19 tau Tg mouse model, demonstrating improved MT density and reduced axonal dystrophy, with a reduction of tau pathology and a trend toward increased hippocampal neuron survival relative to vehicle-treated PS19 mice.
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Tau Pathology Drives Dementia Risk-Associated Gene Networks toward Chronic Inflammatory States and Immunosuppression.

TL;DR: A systematic functional genomic analysis in purified microglia and bulk tissue from mouse and human AD, FTD, and PSP uncovers a complex temporal trajectory of microglial-immune pathways involving the type 1 interferon response associated with tau pathology in the early stages, followed by later signatures of partial immune suppression and, subsequently, the type 2 interferons response.
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Detection of amyloid plaques by radioligands for Aβ40 and Aβ42

TL;DR: A novel radioligand, [125I]TZDM is developed, which binds Aβ fibrils with high affinity, crosses the blood-brain barrier (BBB), and labels amyloid plaques in vivo, and shows differential labeling of SPs in AD brain sections under experimental conditions.
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An insoluble frontotemporal lobar degeneration-associated TDP-43 C-terminal fragment causes neurodegeneration and hippocampus pathology in transgenic mice

TL;DR: It is demonstrated that Camk2a-directed 208 T DP-43 CTF overexpression is sufficient to cause hippocampal pathology and neurodegeneration in vivo, suggesting an active role for TDP- 43 CTFs in the pathogenesis of FTLD-TDP and related TTP-43 proteinopathies.