β-Amyloid Transgenic Alzheimer’s Disease Mouse Model

Table of Contents

Abstract

Presentation

01. Introduction 02. Neuroinflammation Classification 03. Microglial Activation 04. Plaque Microenvironment 05. AD Mouse Model 06. Age & Amyloid 07. Age & Neuroinflammation 08. Age & Microglial Activation 09. Microenvironment Analysis 10. Age & Inflammatory Microenvironment 11. Summary

https://opt003stagmediafiles.blob.core.windows.net/image/594662ca857544aca47419e066dd5b84

https://opt003stagmediafiles.blob.core.windows.net/image/9e9decf5e0ee402c997d09892a543b52

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

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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.