Representative whole brain sections (top panel) and high-magnification view (bottom panel) of APP/PS1 (ARTE10) transgenic and wild-type mice at various time points, stained for β-amyloid (red), Iba-1 (green), GFAP (violet), and DAPI counterstain (blue).
Please note that we provide a link to all of our Alzheimer's disease and other CNS disease models on the last page of this presentation.
References
Willuweit et al., PLoS ONE, 4: e7931, 2009;
doi: 10.1371/journal.pone.0007931
Manook et al., PLoS ONE, 7: e31310, 2012; doi: 10.1371/journal.pone.0031310
Šišková et al., Neuron, 84: 1023-1033, 2014;
doi: 10.1016/j.neuron.2014.10.024
Willuweit et al., Eur. J. Pharm. Sci., 184: 106421, 2023;
doi: 10.1016/j.ejps.2023.106421
To evaluate the performance of our method, we have quantified the inflammatory microenvironment in a mouse model with early-onset and progressive AD-like accumulation of β-amyloid deposits. This transgenic mouse line (ARTE10) is characterized by overexpression of mutated APP and PS1. We observe a reproducible, age-dependent increase in β-amyloid accumulation and neuroinflammation in these mice.