The 5XFAD mouse model of amyloid deposition expresses five familial AD (FAD) mutations that are additive in driving Aβ42 overproduction.

The 5xFAD mice rapidly develop severe amyloid pathology. These mice accumulate high levels of intraneuronal Aβ42 around 1.5 months of age with amyloid deposition in the subiculum and layer 5 of the cortex, both increasing rapidly with age. Plaques spread throughout the hippocampus and cortex by 6 months of age. Gliosis also begins around 2 months, in parallel with plaque deposition. Synapse degeneration is also observed (at approximately 4 months) as well as neuronal loss and deficits in spatial learning (at approximately 4 to 5 months).

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