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Senile plaques and neurofibrillary tangles (NFTs) are major pathological proteinaceous anomalies that occur in the brains of Alzheimer's disease (AD) patients. Motivated by the amyloid hypothesis, animal models exhibiting Aβ deposition have been produced by crossbreeding mice overexpressing human mutant amyloid precursor protein (hAPP) with mice overexpressing mutant PS-1, the latter of which accelerates Aβ deposition in the brain. Most mouse models exhibiting Aβ deposition show memory deficits associated with synaptic plasticity impairments and synapse loss. In this chapter, I introduce the most commonly used amyloid/PS-1 transgenic mouse models that exhibit Aβ deposition and discuss some limitations of using these animal models to understand the devastating condition of AD.

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