Single App knock-in mouse models of Alzheimer's disease
By T. Saito, Y. Matsuba, Naomi Mihira, Jiro Takano, P. Nilsson, S. Itohara, N. Iwata, T. Saido. Nature Neuroscience, 2014
1,116 citations recorded by the source corpus.
Subfields: Biological Psychiatry, Cellular and Molecular Neuroscience, Physiology
View Paper: https://www.semanticscholar.org/paper/9d0f28ef81a12c889b2ffcff9dc6015a0d672a2e
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Biological Psychiatry
In Cellular and Molecular Neuroscience
- Bradley T. Hyman
- D. Selkoe
- V. Perry
- David Attwell
- Lisa Feldman Barrett
- G. Bu
- L. Mucke
- Peter Sterling
In Physiology
- John Hardy
- Thomas Wisniewski
- Bradley T. Hyman
- Eleanor Drummond
- B. de Strooper
- D. Selkoe
- E. Karran
- T. Saido
Citations in the corpus
- APP mouse models for Alzheimer's disease preclinical studies (2017, positive): “Blue: A b ; red: microglia (Iba-1 ); green: astrocyte (GFAP) (Saito et al , 2014 ).”
- Amyloid β oligomers constrict human capillaries in Alzheimer’s disease via signaling to pericytes (2019, background): “AD mice, in which APP with a humanized Ab region containing three AD-related mutations (App) is knocked in (49) to avoid artifacts associated with overexpressing APP, were crossed with NG2-DsRed mice in which pericytes express DsRed (19).”
- Alzheimer’s disease: experimental models and reality (2017, background): “In contrast, initial studies show that more physiological knock-in mouse models develop cognitive impairment many months after plaque development [129], which is more similar to humans.”
- The Major Risk Factors for Alzheimer’s Disease: Age, Sex, and Genes Modulate the Microglia Response to Aβ Plaques (2019, methodology): “time points we used homozygous AppNL-G-F (Saito et al., 2014) mice, backcrossed for at least 2 generations with C57BL/6J mice in the De Strooper lab, and wild-type C57BL/6J mice themselves.”
- The amyloid hypothesis of Alzheimer's disease at 25 years (2016, background): “Recently, mice with gradual Ab plaque accrual have been developed by the judicious use of selective knockin of human mutations into endogenous mouse APP without overexpression (Saito et al, 2014).”
- Temporal Interference Stimulation Enhances Neural Regeneration (2026, unknown): “To test whether AHN can be modulated by TI stimulation with frequency differences Δ f endogenous to the developing brain [ 75 ], we applied TI stimulation to the right hippocampus of a 6-7-month-old APP N-L-GF mouse model [ 76 ].”