Transgenic amyloid models

These models capitalize on the toxicity of amyloid in the brain to induce Alzheimer’s related pathology.

Sylics offers services with several different transgenic amyloid models. The choice of the best model depends on many factors, but all models present with amyloid plaques, inflammation, and cognitive deficits.

Feel free to contact us anytime. One of our scientists will contact you within 24 hours to discuss your research needs.

Transgenic amyloid models that Sylics offers:

APP (Tg2576)



Amyloid oligomers and plaques

Cleavage of the amyloid precursor protein (APP) leads to generation of amyloid beta (Aβ) protein fragments. An early event in the pathology of Alzheimer’s disease (AD) is the oligomerization of Aβ and the formation of amyloid plaques. Most AD patients also have amyloid deposition on the blood vessels, termed cerebral amyloid angiopathy (CAA).

Amyloid models have Aβ plaques, as detected by 6E10 immunofluorescence
The microglial marker IBA1 (green) highlights ramifications and shape of microglia. In transgenic models that (over)express mutated amyloid precursor protein (APP) a portion of the microglia are reactive, leading to a thicker cell bodies with shorter and thicker processes.

Mouse models of amyloid pathology

Mouse models of amyloid pathology (over)express human APP with familial AD-related mutations. These mouse models recapitulate the Aβ aggregation cascade, by expressing higher levels of the toxic Aβ1-40 and Aβ1-42 peptides. This leads to the deposition of plaques in the brain, CAA on the blood vessels, neuroinflammation, and many of the downstream consequences found in AD.

Sylics offers classic transgenic APP and APP/PS1 models. In addition, we offer services with APP targeted replacement (knock-in) humanized mice.

Cognitive deficits

Transgenic APP and APP/PS1 models show robust cognitive impairments, for instance in the Morris Water Maze. Recent studies by others and us show that cognitive impairments can already be detected before plaque onset. In particular, our sensitive CognitionWall™ Discrimination learning task not only detects learning impairments at 6 months (Remmelink et al 2016), but  already at the age of 3 months in APP/PS1 mice, when deficits in the Morris Water Maze are not evident yet.

Amyloid models have learning deficits in the sensitive Cognition Wall
BACE1 inhibitors lower Aβ levels in plasma and brain

Biological readouts

The number and size of amyloid plaques and associated neuroinflammation can be quantified after immunohistochemical (IHC) staining of brain slices. In addition, we measure Aβ levels in the brain, cerebrospinal fluid, and blood using ultra-sensitive immunoassays.

For example, acute treatment with a BACE1 inhibitor, an enzyme critically involved in the generation of toxic Aβ species, effectively reduces the amount of Aβ42 in brain tissue a few hours after treatment.

Drug screening studies in amyloid models

The biological and behavioral phenotypes make transgenic amyloid mice a valuable model of Alzheimer’s disease and suitable for drug-screening studies (Boeddrich et al, 2019). We have previously detected reduction of cognitive deficits after administration of BACE1 inhibitor LY2886721 in our sensitive Cognition Wall behavioral test.

The BACE1 inhibitor LY2886721 was administered 3 hours before the onset of the DL task. This acute inhibition of BACE1, reducing Aβ40 and Aβ42 levels in blood and brain, rescued the behavioral deficit of APP/PS1 mice.

Boeddrich et al. (2019) Cell Chem Biol

Boeddrich A, Babila JT, Wiglenda T, Diez L, Jacob M, Nietfeld W, Huska MR, Haenig C, Groenke N, Buntru A, Blanc E, Meier JC, Vannoni E, Erck C, Friedrich B, Martens H, Neuendorf N, Schnoegl S, Wolfer DP, Loos M, Beule D, Andrade-Navarro MA, Wanker EE. The Anti-amyloid Compound DO1 Decreases Plaque Pathology and Neuroinflammation-Related Expression Changes in 5xFAD Transgenic Mice. Cell Chem Biol. 2019 Jan 17;26(1):109-120.e7. doi: 10.1016/j.chembiol.2018.10.013. Epub 2018 Nov 21. PMID: 30472115.

Keywords: Alzheimer’s disease, amyloid beta, Aβ, Abeta, neuroinflammation

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