The role of neuroinflammation and amyloid in cognitive impairment in an APP/PS1 transgenic mouse model of Alzheimer's disease

APP/PS1 mice exhibited significant memory deficits starting at 5 months, peaking at 12 months.

• Amyloid plaques appeared as early as 3 months, increasing linearly throughout the disease course.
• CD11b-positive microglia and GFAP-positive astrocytes were first detected at 3 months, showing a close association with amyloid plaques.
• The rate of glial activation changes slowed from 12 months, despite a continuous increase in amyloid beta levels.
• Memory impairments in APP/PS1 mice were aggravated over time but reached a plateau by 12 months.

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