Time course of pathological events in models compatible with inflammation hypothesis of Alzheimer’s disease. In the models shown, neuroinflammation starts prior to the appearance of AD related lesions (hp-Tau and Aβ depositions). Animals develop cognitive deficits at variable time points after the induction of neuroinflammation in the respective models. In contrast to the most of transgenic AD animal models, the STZ and p25 Tg models of neuroinflammation feature neurodegeneration. It is noteworthy that the PolyI:C model has the longest time lapse between induction of neuroinflammation and cognitive deficits. Note that the time points do not necessarily represent the actual time of appearance, but the time points when the pathological hallmarks were detected in the respective references (Abbreviations: LPS lipopolysaccharide; PolyI:C polyriboinosinic-polyribocytidilic acid; p25 Tg p25 transgenic model; IL-1β Tg: interleukin-1β transgenic model; ICV-STZ intracerebroventricular streptozotocin model; hp-Tau hyperphosphorylated tau; Aβ amyloid-β).