Mutant presenilins specifically elevate the levels of the 42 residue β-amyloid peptide in vivo: evidence for augmentation of a 42-specific γ secretase
By Joanna L. Jankowsky, Daniel J. Fadale, Jeffrey Anderson, Guilian Xu, V. Gonzales, Nancy A. Jenkins, N. Copeland, Michael K. Lee, L. Younkin, S. Wagner and 2 more. 2004
1,418 citations recorded by the source corpus.
Subfields: Molecular Biology, Pharmacology, Physiology
View Paper: https://www.semanticscholar.org/paper/8faa2f92e09043234a231a254ca8fc9528026805
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Citations in the corpus
- Amyloid β-Induced Neuronal Hyperexcitability Triggers Progressive Epilepsy (2009, methodology): “Similarly, the combination of PS1dE9 with APPswe mutation strongly shifts the gamma-cleavage of A toward A 1– 42 (Jankowsky et al., 2004; Minkeviciene et al., 2008).”
- The Role of Short-Chain Fatty Acids From Gut Microbiota in Gut-Brain Communication (2020, background): “Given that AD has a complex pathology and that therapies that effectively halt the disease progression are still lacking, recent studies have focused on environmental components and diet-based possible prevention strategies by using transgenic animal models (161, 162).”
- Microglial Dysfunction and Defective β-Amyloid Clearance Pathways in Aging Alzheimer's Disease Mice (2008, background): “This process is observed at the age of 8 months and appears to precede or parallel the increase in A levels observed in PS1-APP mice at that age (Jankowsky et al., 2001, 2004).”
- Identification of Amyloid Plaques in Retinas from Alzheimer’s Patients and Noninvasive In Vivo Optical Imaging of Retinal Plaques in a Mouse Model (2010, neutral): “Mice used in this study were genotyped for the presence of the transgenes by PCR, as previously described (Jankowsky et al., 2004b).”
- Pathological roles of MAPK signaling pathways in human diseases. (2010, background): “the three genes encoding amyloid precursor protein (APP) [17], presenilin-1 [18], or presenilin-2 [19], whereas most cases of sporadic AD are thought to result from multiple gene defects [20].”
- Neuronal activity regulates the regional vulnerability to amyloid-β deposition (2011, methodology): “To test this hypothesis, we used 7-month-old APPswe; PSEN1ΔE9 (APP/PS1”