Characterization of amyloid deposition in the APPswe/PS1dE9 mouse model of Alzheimer disease.
By M. Garcia-Alloza, Elissa M. Robbins, Sandy X. Zhang-Nunes, S. M. Purcell, Rebecca A. Betensky, S. Raju, Claudia M. Prada, S. Greenberg, B. Bacskai, Matthew P. Frosch. Neurobiology of Disease, 2006
733 citations recorded by the source corpus.
Transgenic mice carrying disease-linked forms of genes associated with Alzheimer disease often demonstrate deposition of the beta-amyloid as senile plaques and cerebral amyloid angiopathy. We have characterized the natural history of beta-amyloid deposition in APPswe/PS1dE9 mice, a particularly aggressive transgenic mouse model generated with mutant transgenes for APP (APPswe: KM594/5NL) and PS1 (dE9: deletion of exon 9). Ex vivo histochemistry showed Abeta deposition by 4 months with a progressive increase in plaque number up to 12 months and a similar increase of Abeta levels. In vivo multiphoton microscopy at weekly intervals showed increasing beta-amyloid deposition as CAA and plaques. Although first appearing at an early age, CAA progressed at a significantly slower rate than in the Tg2576 mice. The consistent and early onset of beta-amyloid accumulation in the APPswe/PS1dE9 model confirms its utility for studies of biochemical and pathological mechanisms underlying beta-amyloid deposition, as well as exploring new therapeutic treatments.
Subfields: Molecular Biology, Pharmacology, Physiology
View Paper: https://www.semanticscholar.org/paper/3f7904d782183e3f6035ca58d3dbce3475feff49
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Molecular Biology
In Pharmacology
In Physiology
Citations in the corpus
- Identification of Amyloid Plaques in Retinas from Alzheimer’s Patients and Noninvasive In Vivo Optical Imaging of Retinal Plaques in a Mouse Model (2010, unknown): “2g and h), in line with previous descriptions of disease initiation and progression in this strain of AD-Tg mice (Garcia-Alloza et al., 2006).”
- Curcumin labels amyloid pathology in vivo, disrupts existing plaques, and partially restores distorted neurites in an Alzheimer mouse model (2007, methodology): “Other anti-oxidants also show a similar effect in vivo (Garcia-Alloza et al. 2006a), however, in contrast to anti-oxidant treatments, curcumin also reduces dystrophy size in close proximity to the plaques.”
- Amyloid β-Induced Neuronal Hyperexcitability Triggers Progressive Epilepsy (2009, background): “Notably, the time course of A pathology is similar in the mouse line kept on a C57BL/ 6J C3H hybrid background (Garcia-Alloza et al., 2006) as our backcrossed C57BL/6J line (Shemer et al.”
- Aβ plaques lead to aberrant regulation of calcium homeostasis in vivo resulting in structural and functional disruption of neuronal networks (2008, unknown): “5–5 months of age (Garcia-Alloza et al., 2006) whereas the Tg-2576 develop them later—at approximately 14–15 months.”