Table 2.

Characteristics of different Alzheimer’s disease (AD) models.

Model	Mechanism	Main Uses of the Model	Disadvantage
Aβ-induced	Neurotoxicity of Aβ species	Studying Aβ peptide aggregation and deposition, and its acute toxic effect in AD	Not reproducing the progressive neurodegeneration process as an acute model
LPS-induced	Inducing proinflammatory mediators, activating astrocytes and microglia	Simulating neuroinflammation and synaptic/memory dysfunction of AD	Lack of Aβ plaque accumulation and NFT formation
PTZ-induced	Activating free radicals and apoptotosis, modulating neurotransmitters metabolisms	Simulating oxidative damage, motor impairment as well as memory dysfunction of AD	Not replicating the histological hallmarks of AD
Senescence acceleratedmouse	Naturally rapid aging mouse model	Studying the mechanism of age-related spatial learning and memory deficits	Short lifecycle not supporting long-term animal experiments
APP/PS1/tau- transgenic	Aβ accumulation, NFT formation in the brain	Studying the role of APP and tau protein in the development of AD	Lack of APP and tau metabolism changes