Aβ42‐driven cerebral amyloidosis in transgenic mice reveals early and robust pathology
By R. Radde, T. Bolmont, S. Kaeser, Janaky Coomaraswamy, D. Lindau, L. Stoltze, M. Calhoun, F. Jäggi, H. Wolburg, Simon Gengler and 6 more. EMBO Reports, 2006
991 citations recorded by the source corpus.
Subfields: Molecular Biology, Neurology, Physiology
View Paper: https://www.semanticscholar.org/paper/d0b2f6e9abb689ba1e437fbf463ea2b7c7945afe
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In Neurology
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In Physiology
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Citations in the corpus
- Alzheimer’s disease: experimental models and reality (2017, background): “For example, expression of APP and PS1 results in very early plaque formation beginning at approximately 6 weeks [118], while expression of APP and PS1 results in later plaque formation at approximately 6 months [58].”
- Demonstrated brain insulin resistance in Alzheimer's disease patients is associated with IGF-1 resistance, IRS-1 dysregulation, and cognitive decline. (2012, background): “The APP/PS1 mouse model of AD, in which Aβ oligomers are elevated by 2 months (132), shows a 97% increase in basal IRS-1 pS616 in the HF by 7.”
- TREM2 deficiency eliminates TREM2+ inflammatory macrophages and ameliorates pathology in Alzheimer’s disease mouse models (2015, background): “APPPS1-21 (termed APPPS1) mice (provided by M. Jucker, German Center for Neurodegenerative Diseases [DZNE], Tubingen, Germany) express human APP with the Swedish (K670M/N671L) and PSEN1 L166P mutations under control of the Thy1 promoter (Radde et al., 2006).”
- The Diabetes Drug Liraglutide Prevents Degenerative Processes in a Mouse Model of Alzheimer's Disease (2011, background): “…Chemical Industries, catalog #016-20001), goat polyclonal anti-doublecortin (1:200, Santa Cruz Biotechnology, sc-710), or rabbit polyclonal anti-amyloid peptide (1:250, Invitrogen, catalog #71-5800) as shown by Radde et al. (2006), or rabbit antisynaptophysin (1:200, Abcam, catalog #7837- 500).”