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The Journal of Biological Chemistry|March 21, 2003
Presenilin 1 and presenilin 2 have differential effects on the stability and maturation of nicastrin in Mammalian brainFusheng Chen, Anurag Tandon, Nobuo Sanjo, et al.
Neurobiology of Disease|August 11, 2006
Elevated plasma triglyceride levels precede amyloid deposition in Alzheimer's disease mouse models with abundant A beta in plasmaBraydon L Burgess, Sean A McIsaac, Kathryn E Naus, et al.
The American Journal of Pathology|February 1, 2005
Accumulation of filamentous tau in the cerebral cortex of human tau R406W transgenic miceMasaki Ikeda, Mikio Shoji, Toshitaka Kawarai, et al.
Proceedings of the National Academy of Sciences of the United States of America|November 18, 2003
In vivo reduction of amyloid-beta by a mutant copper transporterAmie L Phinney, Bettina Drisaldi, Stephen D Schmidt, et al.
Acta Neuropathologica|March 29, 2020
Diverse, evolving conformer populations drive distinct phenotypes in frontotemporal lobar degeneration caused by the same MAPT-P301L mutationNathalie Daude, Chae Kim, Sang-Gyun Kang, et al.
Plos Pathogens|November 25, 2011
Down-regulation of Shadoo in prion infections traces a pre-clinical event inversely related to PrP(Sc) accumulationDavid Westaway, Sacha Genovesi, Nathalie Daude, et al.
Nature|April 28, 2006
TMP21 is a presenilin complex component that modulates gamma-secretase but not epsilon-secretase activityFusheng Chen, Hiroshi Hasegawa, Gerold Schmitt-Ulms, et al.
Proceedings of the National Academy of Sciences of the United States of America|October 22, 2002
Alleles at the Nicastrin locus modify presenilin 1- deficiency phenotypeRichard Rozmahel, Howard T J Mount, Fusheng Chen, et al.
The Journal of Biological Chemistry|August 27, 2016
Regulation of Amyloid β Oligomer Binding to Neurons and Neurotoxicity by the Prion Protein-mGluR5 ComplexFlavio H Beraldo, Valeriy G Ostapchenko, Fabiana A Caetano, et al.
Biochemistry|August 21, 2007
TgCRND8 amyloid precursor protein transgenic mice exhibit an altered gamma-secretase processing and an aggressive, additive amyloid pathology subject to immunotherapeutic modulationGregory D Van Vickle, Chera L Esh, Walter M Kalback, et al.
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