Mutant presenilins specifically elevate the levels of the 42 residue beta-amyloid peptide in vivo: evidence for augmentation of a 42-specific gamma secretase.
By J. 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. Human Molecular Genetics, 2004
827 citations recorded by the source corpus.
View Paper: https://www.semanticscholar.org/paper/f88a8575e18cfc779fa05958df754750aacbad55
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Citations in the corpus
- The sleep-wake cycle regulates brain interstitial fluid tau in mice and CSF tau in humans (2019, background): “We bred APPswe/PS1δE9 transgenic mice that produce human Aβ (21), to mice that express Cre in excitatory glutamatergic VGLUT2-positive neurons (Vglut2-iresCre mice) (Fig 3A).”
- 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).”
- Complement and Microglia Mediate Early Synapse Loss in Alzheimer Mouse Models (2016, unknown): “C1q was also similarly increased in hippocampus of another model of AD, the APP/PS1 mice (15) (Fig.”
- 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).”