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
The TMEM106B locus and TDP-43 pathology in older persons without FTLD
Lei Yu,Philip L. De Jager,Jingyun Yang,John Q. Trojanowski,David A. Bennett,Julie A. Schneider +5 more
TL;DR: Common variants in TMEM106B serve as a distinct risk factor for TDP-43 pathology in older persons without frontotemporal lobar degeneration and to explore functional pathways that link the risk variants to the pathology, including a GRN mRNA pathway.
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In vivo measurement of plaque burden in a mouse model of Alzheimer's disease
Arijitt Borthakur,Tamar L. Gur,Andrew J. Wheaton,Matthew T. Corbo,John Q. Trojanowski,Virginia M.-Y. Lee,Ravinder Reddy +6 more
TL;DR: An MRI method for directly visualizing amyloid‐β (Aβ) plaques in the APP/PS1 transgenic mouse brain in vivo is demonstrated and it is shown that T1ρ relaxation rate increases progressively with Alzheimer's disease (AD)‐related pathology in the tg mouse brain.
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Brain progranulin expression in GRN-associated frontotemporal lobar degeneration.
Alice Chen-Plotkin,Jiping Xiao,Felix Geser,Maria Martinez-Lage,Murray Grossman,Travis L. Unger,Elisabeth M. Wood,Vivianna M. Van Deerlin,John Q. Trojanowski,Virginia M.-Y. Lee +9 more
TL;DR: It is concluded that GRN mutation carriers have increased levels of mRNA transcript from the normal allele in brain, and proliferation of microglia likely increases progranulin levels in affected regions of the FTLD-TDPbrain, and whether or not these findings underlie the accumulation of TDP-43 pathology in FTLD -TDP linked to GRN mutations remains to be determined.
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Activation of HIPK2 Promotes ER Stress-Mediated Neurodegeneration in Amyotrophic Lateral Sclerosis.
Sebum Lee,Yulei Shang,Stephanie A. Redmond,Anatoly Urisman,Amy A. Tang,Kathy H. Li,Alma L. Burlingame,Ryan A. Pak,Ana Jovičić,Aaron D. Gitler,Jinhua Wang,Nathanael S. Gray,William W. Seeley,Teepu Siddique,Eileen H. Bigio,Virginia M.-Y. Lee,John Q. Trojanowski,Jonah R. Chan,Eric J. Huang +18 more
TL;DR: The identification of homeodomain interacting protein kinase 2 (HIPK2) as the essential link that promotes ER-stress-induced cell death via the IRE1α-ASK1-JNK pathway is reported.
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CSF Apo‑E levels associate with cognitive decline and MRI changes
Jon B. Toledo,Xiao Da,Michael W. Weiner,David A. Wolk,Sharon X. Xie,Steven E. Arnold,Christos Davatzikos,Leslie M. Shaw,John Q. Trojanowski +8 more
TL;DR: It is speculated that increased CSF Apo-E2 or -E3 levels might represent a protective response to injury in AD and may have neuroprotective effects by decreasing neuronal damage independent of tau and amyloid deposition in addition to its effects onAmyloid clearance.